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Review Article | DOI: https://doi.org/10.31579/2690-4861/936
1Department of Gastrointestinal Tract Surgery, Fukushima Medical University.
2Department of Comprehensive Cancer Treatment and Research at Aizu, Fukushima Medical University.
3Department of Surgery, Aizu Medical Center, Fukushima Medical University.
4Department of Surgery, Bange Kousei General Hospital.
5Department of Surgery, Aizu Chuo Hospital.
6Fukushima Medical University.
*Corresponding Author: Masahiko Shibata, Department of Gastrointestinal Tract Surgery, Fukushima Medical University.
Citation: Tomoyuki Momma, Masahiko Shibata, Takahiro Nakajima, Wataru Sakamoto, Teruhide Ishigame, et al, (2025), Immunosuppression and Metabolic Changes in Tumor Microenvironment induced by Myeloid-derived Suppressor Cells and its Relationship with Cancer Cachexia, International Journal of Clinical Case Reports and Reviews, 29(3); DOI:10.31579/2690-4861/936
Copyright: © 2025, Masahiko Shibata. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Received: 01 August 2025 | Accepted: 11 August 2025 | Published: 05 September 2025
Keywords: immunosuppression； cancer immunotherapy; myeloid-derived suppressor cells （MDSC）; cancer cachexia; immunosuppressive cells
Cancer remain a leading cause of death around the world. Although cancer immunotherapy is widely acknowledged as an important treatment option for cancer, myeloid-derived suppressor cells (MDSCs) have been reported to be a major obstacle to immunotherapy. MDSCs are typically absent or present in very low numbers in healthy individuals; however, they have been reported to markedly increase in pathological conditions including cancer. MDSCs exhibit potent immunosuppressive activity in the tumor microenvironment (TME) through multiple mechanisms, including accumulation of immunosuppressive cells, such as regulatory T cells (Tregs) and tumor associated macrophages (TAMs), as well as the production of reactive oxygen and nitrogen species. Cancer cachexia is characterized by weight loss and hypoalbuminemia, and reported to relate with systemic inflammation that is one of the major inducers of MDSCs. An accumulation of MDSCs is observed in patients with cachexia.
Therapeutic modalities targeting MDSCs are under development, with clinical trials currently in progress. Furthermore, in the field of immune-oncology, novel cancer treatments leveraging advanced technologies to target MDSCs have also been reported.
While the survival of cancer patients has been greatly extended in recent years by innovative therapeutic approaches newly introduced to the field, cancers still remain a leading cause of death worldwide [1]. One of the most substantial advances in cancer therapy over the past decades has been the development and success of immune checkpoint inhibitors (ICIs), which can specifically activate immune cells by targeting immune checkpoints, immunosuppressive molecules expressed on immune cells [2].
The process of myelopoiesis involves the differentiation of progenitor cells and myeloid precursors into monocytes, granulocytes, and dendritic cells (DCs) in healthy conditions. Immature myeloid cells (IMC), including myeloid progenitor cells, do not exhibit immunosuppressive activity under normal conditions. However, in chronic inflammatory conditions, such as cancer, chronic infections, and autoimmune diseases, IMC differentiation is suppressed, promoting the accumulation of myeloid-derived suppressor cells (MDSCs), which are pathologically induced immature myeloid cells [3–6]. MDSCs were firstly discovered in 1970s and finally identified and termed in 2007. MDSCs represent a heterogeneous population of IMC that possess various strong immunosuppressive activities involving multiple immunocompetent cells and are significantly accumulated in patients who did not respond to cancer immunotherapies [7,8]. MDSCs are typically absent or present in very low numbers in healthy individuals, but markedly increase in pathological conditions, such as cancer. In cancer, tumors can secrete soluble factors that promote the expansion of MDSCs; therefore, creating a tumor microenvironment (TME) that favors tumor progression by inhibiting effective local immune control of cancer cells. Thus, MDSCs represent a major obstacle to cancer immunotherapy, and have become a target of interest in cancer treatment. Numerous innovative therapies targeting MDSCs have been explored, and various approaches to inhibit MDSC function are currently being evaluated in clinical trials [9]. In this review, we discuss the origin, functions, and metabolic signature s of MDSCs, and highlight the targeting MDSCs as a promising therapeutic approach to suppress their immunosuppressive functions. Additionally, since MDSCs have been reported to be involved in the development of cancer cachexia, we here discuss the functional relationships between the immunological properties of MDSCs and cancer cachexia.
Origin and phenotypes of MDSCs
Heterogeneous and multipotent myeloid cell populations perform diverse specialized functions that are critical for innate immunity against pathogens, maintenance of homeostasis, and coordination of inflammatory responses [10]. These myeloid cell populations were named MDSCs based on their phenotype and immunosuppressive activities, and are classified into two major subsets: monocytic MDSCs (M-MDSCs) expressing CD11b+Ly6GlowLy-6Chigh; and granulocytic or polymorphonuclear MDSCs (G-MDSCs, PMN-MDSCs) expressing CD11b+Ly6G+Ly6Clow [11,12]. Although both populations of MDSCs exhibit strong immunosuppressive activities, G-MDSCs have been proven to expand significantly during tumor progression in cancer patients, G-MDSC is the primary source of immunosuppression that enables tumor escape and tumor progression. In human studies, MDSCs are typically identified by either the expression of the myeloid marker CD33 and low-or-absent expression of HLA-DR, or the expression of CD11b and low/absence of CD14. Recent studies have introduced additional markers including CD15, CD34, CD45, CD84, and IL-4Rα (CD124), to improve the phenotypic characterization of MDSCs [13,14].
Immunosuppressive mechanisms of MDSC s (Figure 1)
Figure 1: MDSCs and its immunosuppression and metabolic characteristics in TME
By pathological activation such as cancer, chronic infections, and autoimmune diseases, differentiation of myeloid cells is suppressed, promoting the accumulation of MDSCs. MDSCs exert strong immunosuppressive effects in the TME through multiple mechanisms, including the accumulation of immunosuppressive cells, such as regulatory T cells (Tregs) and tumor-associated macrophages (TAM), as well as the production of reactive oxygen and nitrogen species, and depletion of L-arginine [9-12]. TME is characterized by VEGF-A-driven impaired perfusion and increased vascular leakage, leading hypoxia, acidity, and interstitial hypertension, resulting in distant metastasis [34-36,75].
HPCs, hematopoietic progenitor cells; CMPs, common myeloid progenitors; GMP, granulocyte macrophage progenitor; MBs, myeloid-like B cells; MDPs, monocyte-DC progenitor; M-MDSCs, monocytic myeloid-derived suppressor cells; G-MDSCs, granulocytic myeloid-derived suppressor cells; ROS, reactive oxygen species; TGF-b, transforming growth factor-beta; NO, nitric oxides; IL-10, interleukin-10; VEGF-A, vascular endothelial growth factor-A
The immune defense system, composed of cytotoxic T cells, natural killer (NK) cells, DCs, and B cells, is essential for tumor control, however its function is impaired by several immunosuppressive factors, including immunosuppressive cells such as MDSCs. MDSCs exert strong immunosuppressive effects in the TME through multiple mechanisms, including the accumulation of immunosuppressive cells, such as regulatory T cells (Tregs) and tumor-associated macrophages, as well as the production of reactive oxygen and nitrogen species.
Interferon（IFN gamma is necessary for MDSCs-mediated induction of Treg cells, and MDSCs have been shown to induce Treg cells through a mechanism mediated by interleukin (IL)-10 [15]. MDSCs and Tregs have been shown to promote the expression of programmed cell death ligand 1 (PD-L1) to induce T cell anergy through interacting with PD-1 on T cells [16,17]. The induction of Tregs has also been demonstrated through chemokines, such as CCL4 and CCL5, secreted by tumor-infiltrating
MDSCs [18]. MDSCs have also been reported to enhance the immunosuppressive functions of Tregs through the direct interactions of CD80 on MDSCs and cytotoxic T-lymphocyte-associated protein (CTLA)-4 [4]. M-MDSCs have also been shown to produce transforming growth factor (TGF)-beta and IL-10, which contribute to immunosuppression of CD8+ T cells. Additionally, MDSCs induce a shift in macrophages toward an M2-like phenotype with immunosuppressive features [19], leading to reduced IL-12 production by M2-like macrophages and promoting a type 2 shift in CD4⁺ T cells within the TME.
It is well known that MDSCs produce reactive oxygen species (ROS), which impair the function of tumor-infiltrating lymphocytes. In addition to their direct toxicity of ROS on immune cells to suppress tumor growth, ROS support the expansion of MDSCs. L-arginine, which is critical for the function of the immune system, can be metabolized in MDSCs by four different enzymes: nitric oxide synthases, including NOS1, NOS2, and NOS3; arginases, including Arg-1 and Arg-2; arginine; glycine aminotransferase; and L-arginine decarboxylase [14].
Metabolic characteristics of MDSCs
As mentioned above, MDSCs promote the differentiations of Tregs and M2-like macrophages by producing TGF-beta and IL-10. These soluble inhibitory mediators also downregulate the expression of the activating receptor NK group 2 member D (NHG2D) in NK cells, thereby abrogating their cytotoxicity [20]. Additionally, MDSCs express several ligands for inhibitory receptors on T cells, promote T cell exhaustion through the T cell immunoglobulin and mucin-domain containing-3 (Tim-3)/Galectin-9 pathway, and terminate Th1 immune responses [21,22].
The Warburg effect is the physiological phenomenon of tumor cells that cancer cells predominantly rely on aerobic glycolysis and lactic acid fermentation for energy generation, differing from the typical glucose metabolism in non-cancerous cells [23]. Specifically, in the TME, cancer cells primarily derive their energy from glycolysis, consuming more glucose and producing higher levels of lactate than non-cancerous cells [24]. Immune competent cells choose aerobic glycolysis due to its rapid energy generation. Moreover, M1 macrophages, for instance, primarily rely on glycolysis, with their proinflammatory functions, including phagocytosis and the production of cytokines such as IL-1 beta, tumor necrosis factor (TNF)-alpha, and IL-6, being directly associated with this metabolic pathway. In contrast, M2 macrophages rely more on fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS) [25]. MDSCs also use aerobic glycolysis to meet their energy demands and support rapid proliferation, thereby creating an immunosuppressive environment that inhibits anti-tumor activities and promotes tumor growth [26,27]. Cytokines including GM-CSF (granulocyte macrophage-colony stimulating factor), as well as IL-6 produced by tumor cells and macrophages, promote glucose uptake and glycolysis in MDSCs, leading to an increased production of lactate. This end product of pyruvate metabolism during aerobic glycolysis plays the critical role of lactate in suppress tumor surveillance [23]. CD8+T cells primarily utilize aerobic glycolysis, while Tregs rely on OXPHOS, which is an important metabolic pathway for immunosuppression and tumor progression. Moreover, in the TME, CD39 and CD73 on tumor cells metabolize ATP (adenosine triphosphate) to adenosine while indoleamine 2,3-dioxygenase (IDO) converts tryptophan into kynurenine, and the resulting accumulation of adenosine and kynurenine supports Tregs [25]. It is also important to focus on adenosine metabolism since emerging evidence have been reported on adenosinergic signaling in immune system. Hypoxia and TGF-beta represent the key drivers of the adenosinergic pathway. A2B, one of the adenosine receptors, predominantly exert immunosuppressive functions, and control some important effects of MDSCs in TME. The adenosine-generating enzymes and possibly adenosine receptors are expressed on MDSCs and regulated by hypoxia and chronic inflammatory factors. MDSCs, therefore, produce adenosine within TME as an additional mechanisms of immunosuppression in TME [28,29]. MDSCs have been reported to produce pro-angiogenic factors, vascular endothelial growth factor (VEGF)-A in a STAT-3 dependent manner and it was shown that adenosine receptor A2B stimulation enhanced the production of VEGF, and pharmacological blockade of A2B reduced tumor angiogenesis, MDSCs accumulation and growth retardation of tumor. This A2B receptor blockade inhibit MDSCs and may be effective as an anti-VEGF agent [30,31].
To meet the high energy demands required for proliferation and the enhancement of immunosuppressive and tumor-promoting functions, MDSCs undergo metabolic reprogramming in the TME, shifting their main energy source from glycolysis to FAO [14]. It has also been reported that MDSCs rely on FAO as the major metabolic pathway for the production of immunosuppressive cytokines. However, the critical factors underlying the metabolic shift between glycolysis and FAO are not yet well understood [32].
Angiogenesis, hypoxia and, MDSCs
Hypoxia is another important feature that is induced not only by metabolic characteristics but also by other factors such as tumor angiogenesis.
In 2011, Hanahan and Weinberg updated the hallmarks of cancer, adding avoiding immune destruction as a new characteristic [33]. Importantly, they included the inhibition of VEGF as a key strategy to suppress the hallmarks of cancer. Tumor vasculature, typically driven by VEGF-A, is structurally and functionally distinct from that of non-malignant tissue, characterized by impaired perfusion and increased vascular leakage, leading hypoxia and acidity in the TME (34). MDSCs are one of the major sources of VEGF-A as well as tumor cells, Tregs, and M2 macrophages. As a result, oxygen and immune competent cells such as CD8+ cells cannot perfuse in the TME, leading to an increase in interstitial pressure due to fluid leakage. Ultimately, even if these lymphocytes circulate within the blood vessels in the TME, they are unable to migrate out of the vessels [35]. There is also a difference between CD8+T cells and Tregs; CD8+T cells utilize aerobic glycolysis and cannot survive in hypoxic conditions, while Tregs are activated in environments with high levels of adenosine and kynurenine. Due to the high vascular permeability and increased interstitial fluid pressure, tumor cells in the TME can easily enter the systemic circulation, resulting in metastasis to distant organs [36].
Another important molecular mechanism is mediated by the transcription factor hypoxia-inducible factor-1 (HIF-1), which is a heterodimer consisting of HIF-1 alpha and HIF-1 beta. HIF-1 alpha induces the upregulation of Arg-1 and increases nitric oxide synthase in hypoxic conditions, thereby enhancing the ability of MDSCs to suppress T cell functions. HIF-1 alpha has been reported to act as a negative regulator of Tregs differentiation and is essential for their immunosuppressive activity [37].
Cancer cachexia, immunosuppression, and MDSCs (Figure 2)
Figure 2: Development of cachexia: Systemic inflammation induced by locally produced inflammatory mediators
MDSCs in cancer patients play an important role in the development of cachexia through the mechanism of inflammatory mediators produced in TME [52-54]. The release of TNF-alpha has been linked directly to muscle wasting. increased levels of IL-1, IL-8 and IL-10 in patients with cancer cachexia result in increased energy expenditure, loss of appetite and muscle atrophy through a mechanism involving multiple organs such as pancreas, brain, liver, muscle and adipose tissue. Insulin plays critical roles of regulating muscle proteolysis and insulin resistance in cancer cachexia, can contribute to muscle wasting [55]. It is also demonstrated that circulating IL-6 reduces dopamine release in the nucleus accumbens, leading lowering motivation and anorexia [59,60].
ROS, reactive oxygen species; TNFa, tumor necrosis factor alpha; IFNg, interferon gamma; TGFb, transforming growth factor beta; VEGF-A, vascular endothelial growth factor-A; IL-1, interleukin-1; IL-4interleukin-4; IL6, interleukin-6; IL-10, interleukin-10; M-MDSCs, monocytic myeloid-derived suppressor cells; G-MDSC, granulocytic myeloid-derived suppressor cells; TAMs, tumor associated macrophages; Tregs, regulatory T cells; FA, fatty acid
Although metabolic features of lipid, glucose, and amino acids have been studied, there have not been reported well on protein metabolism in the biology of MDSCs.
Cachexia is a syndrome that is characterized by weight loss and hypoalbuminemia and cannot be completely recovered by conventional nutritional support. Cancer cachexia specifically arises as a result of cancer [38]. Cancer cachexia is observed in approximately 70% of cancer patients, and accounts for 22% of cancer-related deaths [39]. It is divided into three categories: pre-cachexia, characterized by early clinical and metabolic signs, with < 5> 5% weight loss; and refractory cachexia, which is unresponsive to treatments [39]. Additionally, cancer cachexia has been observed as a negative outcome of cancer treatments, resulting in impaired physical function, resistance to cancer chemotherapies, and poor prognosis [40]. The mechanisms underlying cancer cachexia include tumor cell metabolism, psychiatric effects of the patients, as well as physical and mental changes caused by treatments such as radiotherapy, immunotherapy, and chemotherapy. Among these, the role of the host immune response has been extensively studied for many years and is recognized as essential. We previously focused on the immune alterations observed in cachectic patients, and reported that cancer cachexia is characterized by a Th2-dominant state in CD4⁺ cells, high production of proinflammatory cytokines, and the presence of refractory anti-inflammatory cytokines such as IL-10, as well as refractory immunoregulatory proteins, including soluble receptors for IL-2 and TNF alpha [41-44]. In addition, we measured phytohemagglutinin (PHA)-stimulated lymphocyte proliferation as a measure of cell-mediated immune response, calculating the stimulation index (SI). Our findings revealed that SIs progressively decrease with advancing cancer stages and demonstrate a significant correlation with nutritional parameters. Our previous research also demonstrated that inflammatory indicators, such as neutrophil to lymphocyte ratio (NLR) or C-reactive protein (CRP, clinical indicator of inflammation and IL-6 production), were significantly correlated with nutritional impairments, including decreased serum protein levels, in various cancers [45,46]. Proteins are regulated by the balance between their synthesis and degradation. In cachexia, clinically characterized by hypoproteinemia, metabolic features involving both protein synthesis and degradation have been reported; however, the underlying mechanisms of hypoalbuminemia remain unclear. Moreover, our laboratory has demonstrated that circulating MDSCs (CD11b+, CD14-, CD33+) were increased in patients with various types of cancer, and significant correlations were observed amongst the numbers of MDSCs, systemic inflammation markers, and decreased levels of rapid turnover proteins [47-51]. Among several proinflammatory mediators, we have focused on VEGF-A and IL-17 as inducers of MDSCs [49,51]. Cuenca et al. have reported a novel role of tumor-induced MDSCs in the development of cancer cachexia syndrome [52]. They demonstrated that MDSCs expansion and tumor burden are associated with a decrease in adipose tissue, as well as increases in acute-phase proteins and oxygen consumption, suggesting that MDSCs induces inflammation and play a pivotal role in cancer cachexia (Figure 2). The role of MDSCs-mediated immune system including increased macrophages (TAM) typically shifted to M2, and Tregs, is one of the biggest drivers of cancer cachexia [53]. The release of TNF-alpha has been linked directly to muscle wasting. TNF-a exerts its catabolic function by stimulating the degradation of muscle protein through the activation of E3 ligase pathway [54]. Moreover, increased levels of IL-1, IL-8 and IL-10 in patients with cancer cachexia result in increased energy expenditure, loss of appetite and muscle atrophy through a mechanism involving multiple organs such as pancreas, brain, liver, muscle and adipose tissue [55]. In the mouse model of cancer cachexia, higher loss of adipose tissue and increased consumption of oxygen which is one of the characteristics of cancer cachexia were significantly demonstrated in the mice with expansion of MDSCs compared to those without it [56]. Insulin produced by pancreas and IGF1 (insulin-like growth factor 1) produced by liver activate a cascade of phosphorylation of key-regulators for muscle metabolism. Insulin plays a critical roles of regulating muscle proteolysis and insulin resistance in cancer cachexia, can contribute to muscle wasting [40,57]. IL-6 has been shown to exacerbate cancer cachexia by promoting the wasting of adipose tissues, activating mechanisms that enhance lipolysis and proteolysis through the JAK/STAT3 pathway [58], resulting in weakness and waste of muscle. It is also demonstrated that circulating IL-6 reduces dopamine release in the nucleus accumbens of the brain, leading lowering motivation and anorexia [59]. Zhang and Bonomi reported that anti-cancer therapies targeting MDSCs may not only be effective against immunosuppression but also against cancer cachexia promoted by MDSCs [60],
The anti-aging gene Sirtuin-1 is a NAD+ sensitive deacetylase and mono-transferases, and SIRT1, a member of the sirtuin family, plays a significant role in regulating the creation of ROS [61]. SIRT1 is reported to be critical to systemic inflammation and can control cancer cachexia, and is also demonstrated to control the production of TNF alpha and TGF beta by MDSCs [62,63], thereby the use of SIRT1 activators may be important as therapeutic modalities for cancer cachexia and MDSCs.
Although the mechanisms that induce cancer cachexia has been widely studied, detailed mechanisms and relationship among inflammatory mediators and organs affected in cancer cachexia are not fully clarified yet.
Therapeutic targeting MDSＣs and plasticity of M-MDSC in TME
Multiple trials and approaches to overcome the immunosuppressive actions of MDSCs in cancer have been proposed. Present approaches are divided into 4 categories: 1. Depletion of MDSCs; 2. inhibition of MDSCs immunosuppressive functions; 3. blockade of MDSCs development of recruitment; 4. MDSCs reprogramming or repolarization.
MDSCs are migrated to TME in response to various different growth factors, cytokines and chemokines. The TME is characterized by hypoxia, high concentrations of oxidative factors such as ROS and NO, proinflammatory cytokines, and the metabolic feature of low concentration of glucose and high concentration of lactate. The differentiation and immunosuppressive actions of MDSCs are affected by these conditions [64,65]. Among these factors, hypoxia, especially HIF-1-alpha, which is critical in the induction of M2-type TAMs from monocyte, is important in the TME. Hypoxia also differentiate M-MDSCs to TAMs and provide later events of tumor progression. Colony stimulating factor (CSF)1, CSF2 and VEGF-A produced by tumor are known to be involved in the differentiation of myeloid cells in the TME, and recently, blockade of CSF1/CSFR1 pathway has been demonstrated a significant decrease of the infiltrations of M-MDSCs and TAMs in the TME [66,67]. The CCL2/CCR2 pathway was reported to be necessary in migration of M-MDSCs into TME, and inhibition of CCL2/CCR2 demonstrated significantly decreased infiltration of TAMs and delayed tumor growth [68,69]. Thus, M-MDSC and TAMs showed a closely connected to the differentiation of MDSCs in the TME. M-MDSC represent a potential therapeutic target for cancer therapy, not only because of the ability to control immunosuppression, but also because of high plasticity and differentiation potential [70].
Targeting MDSCs by blocking VEGF-A
Since cancer immunotherapy using ICIs is one of the major treatment modalities for cancer and significant accumulation of MDSCs is often observed in patients with poor responses to such therapies (3,71-73), treatment modalities targeting MDSCs are extremely important in clinical oncology. Hofer et al. described treatment modalities targeting MDSCs, including MDSC depletion, inhibition of MDSC recruitment, blockade of MDSC differentiation into mature immunosuppressive cells, and suppression of MDSC activity. They also summarized related clinical trials. [14]. Li et al. reviewed clinical trials on MDSCs-targeting therapy combined with cancer immunotherapy [13]. VEGF-A possess strong impacts on the induction, activation and proliferation of MDSCs, and there is a close relationship between chronic inflammation underlying MDSCs accumulation and the development of cancer cachexia, as reported in our previous research [36,47,50]. In the present review, we focus particularly on the strategy of blocking VEGF-A signaling in combination with ICI therapies [36,47,50].
There are several characteristics of abnormal vasculature in the TME driven by VEGF-A, inefficient blood supply, increased permeability, dilated and tortuous vessels, decreased pericyte coverage, irregular basement membrane and resultant interstitial hypertension leading tumor expansion and distant metastasis [75]. VEGF-R (receptor)2 is expressed on MDSCs, and VEGF-A secreted by MDSCs induces self-expansion in the TME; thus, targeting the VEGF-A/VEGFR signaling pathway can inhibit the recruitment, accumulation, and proliferation of MDSCs [75].
Currently, clinically available anti-VEGF-A therapies are categorized as follows: 1. neutralizing antibodies to VEGF-A (e.g., bevacizumab), or to VEGF-A receptors (e.g., ramucirumab); 2. tyrosine kinase inhibitors (e.g., sunitinib and sorafenib); and 3. inhibitors of mTOR pathway (e.g., everolimus). Some anti-VEGF-A therapies have been proven to inhibit MDSC accumulation, and bevacizumab-based chemotherapy has been shown in multiple clinical trials to significantly reduce circulating MDSCs and enhance the infiltration of cytotoxic immune cells into the TME [13,76-79]. The increased production of VEGF-A in the patients with cachexia is observed in the clinics and induce massive infiltration and expansion of MDSCs and Tregs. Although it has been reported that blocking VEGF-A induce an immunosupportive condition with normalized vasculature, less MDSCs, and less Treg cells in the TME [72-74], the changes in cachexia have not reported yet.
Conclusions and future directions in MDSCs-targeted therapies
MDSCs are a major obstacle to host immune reaction s in various pathological conditions, including cancer and chronic infection. In chronic infection, therapeutic modalities targeting the metabolism of MDSCs can be beneficial [80], However, compared to cancer, clinical trials in this area remain insufficient. Although MDSCs play a critical role in specific clinical contexts, particularly in autoimmune diseases and pregnancy [4], therapeutic strategies aimed at inducing MDSCs in these patients have not been thoroughly explored or discussed. Additionally, the relationships of MDSCs with cancer cachexia is addressed in this review.
Currently, therapies targeting MDSCs are primarily focused on cancer, and evidence from basic research in this field, as well as clinical benefits of MDSCs-targeting treatments such as anti-VEGF-A therapies including ICIs, has been accumulating [13,14]. As novel anticancer treatment modalities, gene modification of MDSCs by CRISPR (clustered regularly interspaced short palindromic repeats) technology has been demonstrated to eliminate immunosuppressive activities, and CRISPR-loaded nanoparticles may decrease MDSC-derived immunosuppression [81-83]. Although these technologies are currently utilized in basic and translational studies, their future development is expected to expand into clinical applications.
Conclusively, MDSCs possess variety of biological functions leading to immunosuppression, tumor progression and nutritional damages in patients with cancer. Clinical studies of MDSCs-targeting strategies have just started and we hope new therapeutic modalities will arise in the clinic soon.
MS, KK, TN and ST were involved in the conceptualization, WS, TI, MT, TY, NI and TM contributed to the literature search, TS, KG and MS wrote the manuscript draft, and KK reviewed and edited.
The authors declare that they have no competing interests.
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I would like to give my testimony in the support I have got by the peer review process and to support the editorial office where they were of asset to support young author like me to be encouraged to publish their work in your respected journal and globalize and share knowledge across the globe. I really give my great gratitude to your journal and the peer review including the editorial office.
I am delighted to publish our manuscript entitled "A Perspective on Cocaine Induced Stroke - Its Mechanisms and Management" in the Journal of Neuroscience and Neurological Surgery. The peer review process, support from the editorial office, and quality of the journal are excellent. The manuscripts published are of high quality and of excellent scientific value. I recommend this journal very much to colleagues.
Dr.Tania Muñoz, My experience as researcher and author of a review article in The Journal Clinical Cardiology and Interventions has been very enriching and stimulating. The editorial team is excellent, performs its work with absolute responsibility and delivery. They are proactive, dynamic and receptive to all proposals. Supporting at all times the vast universe of authors who choose them as an option for publication. The team of review specialists, members of the editorial board, are brilliant professionals, with remarkable performance in medical research and scientific methodology. Together they form a frontline team that consolidates the JCCI as a magnificent option for the publication and review of high-level medical articles and broad collective interest. I am honored to be able to share my review article and open to receive all your comments.
“The peer review process of JPMHC is quick and effective. Authors are benefited by good and professional reviewers with huge experience in the field of psychology and mental health. The support from the editorial office is very professional. People to contact to are friendly and happy to help and assist any query authors might have. Quality of the Journal is scientific and publishes ground-breaking research on mental health that is useful for other professionals in the field”.
Dear editorial department: On behalf of our team, I hereby certify the reliability and superiority of the International Journal of Clinical Case Reports and Reviews in the peer review process, editorial support, and journal quality. Firstly, the peer review process of the International Journal of Clinical Case Reports and Reviews is rigorous, fair, transparent, fast, and of high quality. The editorial department invites experts from relevant fields as anonymous reviewers to review all submitted manuscripts. These experts have rich academic backgrounds and experience, and can accurately evaluate the academic quality, originality, and suitability of manuscripts. The editorial department is committed to ensuring the rigor of the peer review process, while also making every effort to ensure a fast review cycle to meet the needs of authors and the academic community. Secondly, the editorial team of the International Journal of Clinical Case Reports and Reviews is composed of a group of senior scholars and professionals with rich experience and professional knowledge in related fields. The editorial department is committed to assisting authors in improving their manuscripts, ensuring their academic accuracy, clarity, and completeness. Editors actively collaborate with authors, providing useful suggestions and feedback to promote the improvement and development of the manuscript. We believe that the support of the editorial department is one of the key factors in ensuring the quality of the journal. Finally, the International Journal of Clinical Case Reports and Reviews is renowned for its high- quality articles and strict academic standards. The editorial department is committed to publishing innovative and academically valuable research results to promote the development and progress of related fields. The International Journal of Clinical Case Reports and Reviews is reasonably priced and ensures excellent service and quality ratio, allowing authors to obtain high-level academic publishing opportunities in an affordable manner. I hereby solemnly declare that the International Journal of Clinical Case Reports and Reviews has a high level of credibility and superiority in terms of peer review process, editorial support, reasonable fees, and journal quality. Sincerely, Rui Tao.
Clinical Cardiology and Cardiovascular Interventions I testity the covering of the peer review process, support from the editorial office, and quality of the journal.
Clinical Cardiology and Cardiovascular Interventions, we deeply appreciate the interest shown in our work and its publication. It has been a true pleasure to collaborate with you. The peer review process, as well as the support provided by the editorial office, have been exceptional, and the quality of the journal is very high, which was a determining factor in our decision to publish with you.
The peer reviewers process is quick and effective, the supports from editorial office is excellent, the quality of journal is high. I would like to collabroate with Internatioanl journal of Clinical Case Reports and Reviews journal clinically in the future time.
Clinical Cardiology and Cardiovascular Interventions, I would like to express my sincerest gratitude for the trust placed in our team for the publication in your journal. It has been a true pleasure to collaborate with you on this project. I am pleased to inform you that both the peer review process and the attention from the editorial coordination have been excellent. Your team has worked with dedication and professionalism to ensure that your publication meets the highest standards of quality. We are confident that this collaboration will result in mutual success, and we are eager to see the fruits of this shared effort.
Dear Dr. Jessica Magne, Editorial Coordinator 0f Clinical Cardiology and Cardiovascular Interventions, I hope this message finds you well. I want to express my utmost gratitude for your excellent work and for the dedication and speed in the publication process of my article titled "Navigating Innovation: Qualitative Insights on Using Technology for Health Education in Acute Coronary Syndrome Patients." I am very satisfied with the peer review process, the support from the editorial office, and the quality of the journal. I hope we can maintain our scientific relationship in the long term.
Dear Monica Gissare, - Editorial Coordinator of Nutrition and Food Processing. ¨My testimony with you is truly professional, with a positive response regarding the follow-up of the article and its review, you took into account my qualities and the importance of the topic¨.
Dear Dr. Jessica Magne, Editorial Coordinator 0f Clinical Cardiology and Cardiovascular Interventions, The review process for the article “The Handling of Anti-aggregants and Anticoagulants in the Oncologic Heart Patient Submitted to Surgery” was extremely rigorous and detailed. From the initial submission to the final acceptance, the editorial team at the “Journal of Clinical Cardiology and Cardiovascular Interventions” demonstrated a high level of professionalism and dedication. The reviewers provided constructive and detailed feedback, which was essential for improving the quality of our work. Communication was always clear and efficient, ensuring that all our questions were promptly addressed. The quality of the “Journal of Clinical Cardiology and Cardiovascular Interventions” is undeniable. It is a peer-reviewed, open-access publication dedicated exclusively to disseminating high-quality research in the field of clinical cardiology and cardiovascular interventions. The journal's impact factor is currently under evaluation, and it is indexed in reputable databases, which further reinforces its credibility and relevance in the scientific field. I highly recommend this journal to researchers looking for a reputable platform to publish their studies.
Dear Editorial Coordinator of the Journal of Nutrition and Food Processing! "I would like to thank the Journal of Nutrition and Food Processing for including and publishing my article. The peer review process was very quick, movement and precise. The Editorial Board has done an extremely conscientious job with much help, valuable comments and advices. I find the journal very valuable from a professional point of view, thank you very much for allowing me to be part of it and I would like to participate in the future!”
Dealing with The Journal of Neurology and Neurological Surgery was very smooth and comprehensive. The office staff took time to address my needs and the response from editors and the office was prompt and fair. I certainly hope to publish with this journal again.Their professionalism is apparent and more than satisfactory. Susan Weiner
My Testimonial Covering as fellowing: Lin-Show Chin. The peer reviewers process is quick and effective, the supports from editorial office is excellent, the quality of journal is high. I would like to collabroate with Internatioanl journal of Clinical Case Reports and Reviews.
My experience publishing in Psychology and Mental Health Care was exceptional. The peer review process was rigorous and constructive, with reviewers providing valuable insights that helped enhance the quality of our work. The editorial team was highly supportive and responsive, making the submission process smooth and efficient. The journal's commitment to high standards and academic rigor makes it a respected platform for quality research. I am grateful for the opportunity to publish in such a reputable journal.
My experience publishing in International Journal of Clinical Case Reports and Reviews was exceptional. I Come forth to Provide a Testimonial Covering the Peer Review Process and the editorial office for the Professional and Impartial Evaluation of the Manuscript.
I would like to offer my testimony in the support. I have received through the peer review process and support the editorial office where they are to support young authors like me, encourage them to publish their work in your esteemed journals, and globalize and share knowledge globally. I really appreciate your journal, peer review, and editorial office.
Dear Agrippa Hilda- Editorial Coordinator of Journal of Neuroscience and Neurological Surgery, "The peer review process was very quick and of high quality, which can also be seen in the articles in the journal. The collaboration with the editorial office was very good."
I would like to express my sincere gratitude for the support and efficiency provided by the editorial office throughout the publication process of my article, “Delayed Vulvar Metastases from Rectal Carcinoma: A Case Report.” I greatly appreciate the assistance and guidance I received from your team, which made the entire process smooth and efficient. The peer review process was thorough and constructive, contributing to the overall quality of the final article. I am very grateful for the high level of professionalism and commitment shown by the editorial staff, and I look forward to maintaining a long-term collaboration with the International Journal of Clinical Case Reports and Reviews.
To Dear Erin Aust, I would like to express my heartfelt appreciation for the opportunity to have my work published in this esteemed journal. The entire publication process was smooth and well-organized, and I am extremely satisfied with the final result. The Editorial Team demonstrated the utmost professionalism, providing prompt and insightful feedback throughout the review process. Their clear communication and constructive suggestions were invaluable in enhancing my manuscript, and their meticulous attention to detail and dedication to quality are truly commendable. Additionally, the support from the Editorial Office was exceptional. From the initial submission to the final publication, I was guided through every step of the process with great care and professionalism. The team's responsiveness and assistance made the entire experience both easy and stress-free. I am also deeply impressed by the quality and reputation of the journal. It is an honor to have my research featured in such a respected publication, and I am confident that it will make a meaningful contribution to the field.
"I am grateful for the opportunity of contributing to [International Journal of Clinical Case Reports and Reviews] and for the rigorous review process that enhances the quality of research published in your esteemed journal. I sincerely appreciate the time and effort of your team who have dedicatedly helped me in improvising changes and modifying my manuscript. The insightful comments and constructive feedback provided have been invaluable in refining and strengthening my work".
I thank the ‘Journal of Clinical Research and Reports’ for accepting this article for publication. This is a rigorously peer reviewed journal which is on all major global scientific data bases. I note the review process was prompt, thorough and professionally critical. It gave us an insight into a number of important scientific/statistical issues. The review prompted us to review the relevant literature again and look at the limitations of the study. The peer reviewers were open, clear in the instructions and the editorial team was very prompt in their communication. This journal certainly publishes quality research articles. I would recommend the journal for any future publications.
Dear Jessica Magne, with gratitude for the joint work. Fast process of receiving and processing the submitted scientific materials in “Clinical Cardiology and Cardiovascular Interventions”. High level of competence of the editors with clear and correct recommendations and ideas for enriching the article.
We found the peer review process quick and positive in its input. The support from the editorial officer has been very agile, always with the intention of improving the article and taking into account our subsequent corrections.
My article, titled 'No Way Out of the Smartphone Epidemic Without Considering the Insights of Brain Research,' has been republished in the International Journal of Clinical Case Reports and Reviews. The review process was seamless and professional, with the editors being both friendly and supportive. I am deeply grateful for their efforts.
To Dear Erin Aust – Editorial Coordinator of Journal of General Medicine and Clinical Practice! I declare that I am absolutely satisfied with your work carried out with great competence in following the manuscript during the various stages from its receipt, during the revision process to the final acceptance for publication. Thank Prof. Elvira Farina
Dear Jessica, and the super professional team of the ‘Clinical Cardiology and Cardiovascular Interventions’ I am sincerely grateful to the coordinated work of the journal team for the no problem with the submission of my manuscript: “Cardiometabolic Disorders in A Pregnant Woman with Severe Preeclampsia on the Background of Morbid Obesity (Case Report).” The review process by 5 experts was fast, and the comments were professional, which made it more specific and academic, and the process of publication and presentation of the article was excellent. I recommend that my colleagues publish articles in this journal, and I am interested in further scientific cooperation. Sincerely and best wishes, Dr. Oleg Golyanovskiy.
Dear Ashley Rosa, Editorial Coordinator of the journal - Psychology and Mental Health Care. " The process of obtaining publication of my article in the Psychology and Mental Health Journal was positive in all areas. The peer review process resulted in a number of valuable comments, the editorial process was collaborative and timely, and the quality of this journal has been quickly noticed, resulting in alternative journals contacting me to publish with them." Warm regards, Susan Anne Smith, PhD. Australian Breastfeeding Association.
Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. I appreciate the journal (JCCI) editorial office support, the entire team leads were always ready to help, not only on technical front but also on thorough process. Also, I should thank dear reviewers’ attention to detail and creative approach to teach me and bring new insights by their comments. Surely, more discussions and introduction of other hemodynamic devices would provide better prevention and management of shock states. Your efforts and dedication in presenting educational materials in this journal are commendable. Best wishes from, Farahnaz Fallahian.
Dear Maria Emerson, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. I am delighted to have published our manuscript, "Acute Colonic Pseudo-Obstruction (ACPO): A rare but serious complication following caesarean section." I want to thank the editorial team, especially Maria Emerson, for their prompt review of the manuscript, quick responses to queries, and overall support. Yours sincerely Dr. Victor Olagundoye.
Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. Many thanks for publishing this manuscript after I lost confidence the editors were most helpful, more than other journals Best wishes from, Susan Anne Smith, PhD. Australian Breastfeeding Association.
Dear Agrippa Hilda, Editorial Coordinator, Journal of Neuroscience and Neurological Surgery. The entire process including article submission, review, revision, and publication was extremely easy. The journal editor was prompt and helpful, and the reviewers contributed to the quality of the paper. Thank you so much! Eric Nussbaum, MD
Dr Hala Al Shaikh This is to acknowledge that the peer review process for the article ’ A Novel Gnrh1 Gene Mutation in Four Omani Male Siblings, Presentation and Management ’ sent to the International Journal of Clinical Case Reports and Reviews was quick and smooth. The editorial office was prompt with easy communication.
Dear Erin Aust, Editorial Coordinator, Journal of General Medicine and Clinical Practice. We are pleased to share our experience with the “Journal of General Medicine and Clinical Practice”, following the successful publication of our article. The peer review process was thorough and constructive, helping to improve the clarity and quality of the manuscript. We are especially thankful to Ms. Erin Aust, the Editorial Coordinator, for her prompt communication and continuous support throughout the process. Her professionalism ensured a smooth and efficient publication experience. The journal upholds high editorial standards, and we highly recommend it to fellow researchers seeking a credible platform for their work. Best wishes By, Dr. Rakhi Mishra.
Dear Jessica Magne, Editorial Coordinator, Clinical Cardiology and Cardiovascular Interventions, Auctores Publishing LLC. The peer review process of the journal of Clinical Cardiology and Cardiovascular Interventions was excellent and fast, as was the support of the editorial office and the quality of the journal. Kind regards Walter F. Riesen Prof. Dr. Dr. h.c. Walter F. Riesen.
Dear Ashley Rosa, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews, Auctores Publishing LLC. Thank you for publishing our article, Exploring Clozapine's Efficacy in Managing Aggression: A Multiple Single-Case Study in Forensic Psychiatry in the international journal of clinical case reports and reviews. We found the peer review process very professional and efficient. The comments were constructive, and the whole process was efficient. On behalf of the co-authors, I would like to thank you for publishing this article. With regards, Dr. Jelle R. Lettinga.
Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, I would like to express my deep admiration for the exceptional professionalism demonstrated by your journal. I am thoroughly impressed by the speed of the editorial process, the substantive and insightful reviews, and the meticulous preparation of the manuscript for publication. Additionally, I greatly appreciate the courteous and immediate responses from your editorial office to all my inquiries. Best Regards, Dariusz Ziora
Dear Chrystine Mejia, Editorial Coordinator, Journal of Neurodegeneration and Neurorehabilitation, Auctores Publishing LLC, We would like to thank the editorial team for the smooth and high-quality communication leading up to the publication of our article in the Journal of Neurodegeneration and Neurorehabilitation. The reviewers have extensive knowledge in the field, and their relevant questions helped to add value to our publication. Kind regards, Dr. Ravi Shrivastava.
Dear Clarissa Eric, Editorial Coordinator, Journal of Clinical Case Reports and Studies, Auctores Publishing LLC, USA Office: +1-(302)-520-2644. I would like to express my sincere appreciation for the efficient and professional handling of my case report by the ‘Journal of Clinical Case Reports and Studies’. The peer review process was not only fast but also highly constructive—the reviewers’ comments were clear, relevant, and greatly helped me improve the quality and clarity of my manuscript. I also received excellent support from the editorial office throughout the process. Communication was smooth and timely, and I felt well guided at every stage, from submission to publication. The overall quality and rigor of the journal are truly commendable. I am pleased to have published my work with Journal of Clinical Case Reports and Studies, and I look forward to future opportunities for collaboration. Sincerely, Aline Tollet, UCLouvain.
Dear Ms. Mayra Duenas, Editorial Coordinator, International Journal of Clinical Case Reports and Reviews. “The International Journal of Clinical Case Reports and Reviews represented the “ideal house” to share with the research community a first experience with the use of the Simeox device for speech rehabilitation. High scientific reputation and attractive website communication were first determinants for the selection of this Journal, and the following submission process exceeded expectations: fast but highly professional peer review, great support by the editorial office, elegant graphic layout. Exactly what a dynamic research team - also composed by allied professionals - needs!" From, Chiara Beccaluva, PT - Italy.
Dear Maria Emerson, Editorial Coordinator, we have deeply appreciated the professionalism demonstrated by the International Journal of Clinical Case Reports and Reviews. The reviewers have extensive knowledge of our field and have been very efficient and fast in supporting the process. I am really looking forward to further collaboration. Thanks. Best regards, Dr. Claudio Ligresti
Dear Chrystine Mejia, Editorial Coordinator, Journal of Neurodegeneration and Neurorehabilitation. “The peer review process was efficient and constructive, and the editorial office provided excellent communication and support throughout. The journal ensures scientific rigor and high editorial standards, while also offering a smooth and timely publication process. We sincerely appreciate the work of the editorial team in facilitating the dissemination of innovative approaches such as the Bonori Method.” Best regards, Dr. Matteo Bonori.
