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Disruption of CXCR2-Mediated MDSC Tumor Trafficking Enhances Anti-PD1 Efficacy
Open accessAbstract
Preventing trafficking of myeloid-derived suppressor cells to the tumor site enhances the efficiency of checkpoint blockade.
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“Notably, data from various mouse models indicate that disrupting the CXCR1/2–MDSC axis in tumours is therapeutically efficacious across a wide variety of solid cancers166–172.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [168]
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BackgroundBlockade of CCL2 enhances immunotherapeutic effect of anti-PD1 in lung cancer
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“The reduction of G-MDSC delayed tumor growth and significantly improved the in vivo efficacy of antiPD1 treatment [20].”
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“trafficking and resistance to immunotherapy (51).”
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“It is also known that autologous antitumor immunity could be achieved by silencing regulatory immune cells such as Tregs and myeloid-derived suppressor cells (MDSCs) [19,20].”
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“In addition, decreasing the expression of IL8 has been shown to be beneficial for immune checkpoint blockade therapy, such as anti-PD-L1 and anti-CTLA-4 (19, 20), and the combination of CXCR2-blocking antibody or CXCR2 antagonist with anti-PD-L1 antibody showed more effective tumor growth inhibition (56).”
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“Similarly, in a murine model of rhabdomyosarcoma (RMS), treatment with an anti-CXCR2 antibody sensitized tumors to anti-PD1 treatment [45].”
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“In fact, eradicating MDSC infiltration by blocking CXCR2 also impaired NET formation and sensitized tumors to immune-checkpoint inhibitors (45).”
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“Interestingly, with regards to an increase in Gr-1C PMN-MDSCs, two recent investigations demonstrated that eradication or suppression of MDSC population enhances checkpoint blockade efficacy.(8,21) While the immune mediators of clinical irAEs remain unclear or noted as lymphocytic, this is the first report to show org…”
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“[70] developed a model of rhabdomyosarcoma in mice and found that the accumulation of CXCR2CD11bLy6G MDSCs in the tumor bed was the root cause limiting the efficacy of PD1 checkpoint blockade in cancer.”
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“[56] demonstrated that the accumulation of myeloid-derived suppressor cells in the tumor bed can limit the efficacy of checkpoint blockade in cancer.”
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“Blocking CXCR2 has limited the recruitment of PMN-MDSCs and enhanced the efficacy of anti-PD-1 therapy or chemotherapy in preclinical studies.(94,95) However, there has been no clinical development of inhibitors of these chemokine receptors in HCC.”
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“Other approaches include blocking the chemokine receptor CXCR2 to prevent MDSC recruitment into the tumor, which sensitizes a mouse model of rhabdomyosarcoma to anti-PD-1 (66), and using the repurposed drug ibrutinib which inhibits MDSCs and sensitizes murine breast cancer models to anti-PD-L1 (67, 68).”
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“Other treatment-related changes include a reduction of Gr1þCD11bþ myeloid-derived suppressor cells (MDSC) in the tumor and spleen and the upregulation of PD-L1 on MDSCs.”
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“Moreover, the proliferation of CXCR2CD11bLy6G MDSCs induced by CXCR2 ligands produced by tumor cells inhibits T cell proliferation by L-arginine depletion and exerts local immunosuppressive effects.(134) Furthermore, MDSCs can inhibit the host antitumor immune response by inducing Tregs.”
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“Inconsistent with these observations, targeting chemokine receptors with neutralizing antibodies endow a more sensitized phenotype and enhance responses to immune checkpoint blockades [11,12].”
BackgroundDynamics of Neutrophils-to-Lymphocyte Ratio Predict Outcomes of PD-1/PD-L1 Blockade
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“MDSCs can adopt multiple mechanisms to induce immunosuppression, including production of arginase 1 and inducible nitric oxide synthase, leading to T-cell inhibition [19, 20].”
BackgroundNeutrophil interactions with T cells, platelets, endothelial cells, and of course tumor cells
Segal, B. H., Giridharan, T., Suzuki, S., Khan, A. N. H., Zsíros, E., Emmons, T. R., Yaffe, M. B., Gankema, A. A. F., Hoogeboom, M., Goetschalckx, I., et al. (2022) · Immunological Reviews · doi:10.1111/imr.13178 · Cited by 67
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“As M-MDSCs are actively recruited to primary and metastatic tumour sites by several chemokine-associated circuits that are controlled primarily by C-C motif chemokine ligand (CCL)2 and CCL5, several antibodies and small molecules targeting this cell recruitment axis are being studied in different clinical trials for u…”
BackgroundMitchell, K. G., Diao, L., Karpinets, T. V., Negrao, M. V., Tran, H. T., Parra, E. R., Corsini, E. M., Reuben, A., Federico, L., Bernatchez, C., et al. (2020) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2019-000405 · Cited by 64
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“The best understood chemokines are the CXCR and CCR families (Debnath et al., 2013; Highfill et al., 2014; Katoh et al., 2013; Peled et al., 2014; Weitzenfeld & Ben-Baruch, 2014).”
BackgroundZhao, Y., Shen, X., Cao, K., Ding, J., Kang, X., Guan, W.-X., Ding, Y.-T., Liu, B.-R., & Du, J. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00282 · Cited by 61
“To explore whether the prolongation of allograft seen in Dex-MDSCs treated mice was due to an enhanced migration of MDSCs, we first assessed the expression of CXCR2, which was implicated in mediating MDSCs recruitment into local inflammatory and tumor sites (19, 20).”
BackgroundTakeyama, Y., Kato, M., Tamada, S., Azuma, Y., Shimizu, Y., Iguchi, T., Yamasaki, T., Gi, M., Wanibuchi, H., & Nakatani, T. (2020) · Cancer Letters · doi:10.1016/j.canlet.2020.03.013 · Cited by 61
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“We did not observe a reduction in CD45+CD11b+GR1hi neutrophils in Osmr-KO tumors by FACS analysis (Supplemental Figure 13, A and B), suggesting that Ly6G staining in MMTV-PyMT Osmr-KO tumors may be marking neutrophils but also other myeloid-derived cells such as MDSCs (36, 37).”
3D Tumor Spheroid and Organoid to Model Tumor Microenvironment for Cancer Immunotherapy
Zhu, Y., Kang, E., Wilson, M., Basso, T., Chen, E., Yu, Y., & Li, Y.-R. (2022) · Organoids · doi:10.3390/organoids1020012 · Cited by 63
“Tumor trafficking of MDSCs is also inhibited by CXCR2 deficiency or anti-CXCR2 monoclonal antibody therapy, increasing the efficacy of anti PD-1 therapy through targeting of the CXCL5-CXCR2 signaling pathway [18,19,21].”
BackgroundSmall molecules as theranostic agents in cancer immunology
Li, J., Valkenburgh, J. S. V., Hong, X., Conti, P. S., Zhang, X., & Chen, K. (2019) · Theranostics · doi:10.7150/thno.37218 · Cited by 61
“In addition, CXCR2 also modulates MDSCs migrations and mediates local immunosuppression [71].”
BackgroundTargeting of SLC25A22 boosts the immunotherapeutic response in KRAS-mutant colorectal cancer
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“Tumor trafficking of myeloid-derived suppressor cells is inhibited by CXCR2 deficiency in a mouse model of rhabdomyosarcoma [35] and data from a mouse model of colitis-associated cancer suggests that CXCR2 is required for recruitment of myeloid-derived suppressor cells [24,36].”
BackgroundTherapeutic inhibition of CXCR1/2: where do we stand?
Sitaru, S., Budke, A., Bertini, R., & Sperandio, M. (2023) · Internal and Emergency Medicine · doi:10.1007/s11739-023-03309-5 · Cited by 58
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“CXCL1 expression drives recruitment of CXCR2 PMN-MDSCs in multiple tumor models(9,37,38), but control of migration of myeloid cells by semaphorin family members has also been demonstrated in other models(30,31).”
BackgroundTumor control via targeting PD-L1 with chimeric antigen receptor modified NK cells
Robbins, Y. L., Greene, S., Friedman, J., Clavijo, P. E., Waes, C. V., Fabian, K. P., Padget, M. R., Sater, H. A., Lee, J. H., Soon‐Shiong, P., et al. (2020) · eLife · doi:10.7554/elife.54854 · Cited by 57
“We and others have demonstrated that elimination of myeloid cells or inhibition of their trafficking into 301 tumors has little effect as a monotherapy but enhances T cell cell-based immunotherapy when used in 302 combination(33-35).”
BackgroundChen, I. X., Newcomer, K., Pauken, K. E., Juneja, V. R., Naxerova, K., Wu, M. W., Pinter, M., Sen, D. R., Singer, M., Sharpe, A. H., et al. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2002806117 · Cited by 55
Myeloid Cell Mediated Immune Suppression in Pancreatic Cancer
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Effects of helicobacter pylori on tumor microenvironment and immunotherapy responses
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“Recent studies have revealed that depletion [11-14] or inhibition [15-17] of MDSCs substantially augments antitumor responses, highlighting the promise of MDSC targeting strategies for cancer therapy.”
Therapeutic applications of the cancer immunoediting hypothesis
Desai, R. R., Coxon, A. T., & Dunn, G. P. (2021) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2021.03.002 · Cited by 59
Moses, K., Klein, J. C., Männ, L., Grüneboom, A., Gunzer, M., & Brandau, S. (2016) · Journal of Leukocyte Biology · doi:10.1189/jlb.1hi0715-289r · Cited by 58
“For murine Ly-6G myeloid cells, a predominant role for CXCR2 and its ligands was suggested, and this was further supported by studies using human neutrophils [14, 15, 17, 19, 32].”
BackgroundGhayad, S. E., Rammal, G., Ghamloush, F., Basma, H., Nasr, R., Diab‐Assaf, M., Chelala, C., & Saab, R. H. (2016) · Scientific Reports · doi:10.1038/srep37088 · Cited by 57
DeNardo, D. G., Galkin, A., Dupont, J., Zhou, L., & Bendell, J. (2021) · Journal for ImmunoTherapy of Cancer · doi:10.1136/jitc-2021-003005 · Cited by 53
“31 32 Colony-stimulating factor 1 receptor (CSF-1R), 37 phosphoinositide 3- kinase-gamma (PI3K γ ), 38 and integrin 39 signaling pathways also play an important role in MDSC migration and/or TAM polarization in the TME.”
Progress and Opportunities for Immune Therapeutics in Osteosarcoma
Lettieri, C. K., Appel, N., Labban, N., Lussier, D. M., Blattman, J. N., & Hingorani, P. (2016) · Immunotherapy · doi:10.2217/imt-2016-0048 · Cited by 54
Guan, Y., Zhang, R., Peng, Z., Dong, D., Wei, G., & Wang, Y. (2017) · Journal of bone oncology · doi:10.1016/j.jbo.2017.10.002 · Cited by 54
“G-MDSC reduction delayed tumor growth and significantly improved the efficacy of anti-PD1 treatment [23].”
BackgroundOvercoming immunotherapeutic resistance by targeting the cancer inflammation cycle
Wattenberg, M. M., & Beatty, G. L. (2020) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2020.01.002 · Cited by 54
“In mouse models of sarcoma and pancreatic cancer, inhibition of CXCR2 in combination with anti-PD1 therapy reduces metastases and improves the efficacy of anti-PD1 immunotherapy [96, 158].”
BackgroundThe emerging role of myeloid-derived suppressor cells in radiotherapy
Kang, C., Jeong, S., Song, S. Y., & Choi, E. K. (2020) · Radiation Oncology Journal · doi:10.3857/roj.2019.00640 · Cited by 55
“Recent studies have shown that targeting CXCR2 inhibits recruitment of PMN-MDSCs and enhances immunotherapy in preclinical studies [62,63].”
BackgroundPratt, H. G., Steinberger, K. J., Mihalik, N. E., Ott, S., Whalley, T., Szomolay, B., Boone, B. A., & Eubank, T. D. (2021) · Cancers · doi:10.3390/cancers14010194 · Cited by 58
“For example, NETs can exclude CD8+ T cells from the TME serving as a physical barrier to T cell infiltration [3,4] and can specifically block NK cell or CD8+ T cell mediated cytotoxicity of tumor cells [69].”
BackgroundPreclinical models for drug discovery for metastatic disease
Wakefield, L. M., Agarwal, S., & Tanner, K. (2023) · Cell · doi:10.1016/j.cell.2023.02.026 · Cited by 55
Tumoral EHF predicts the efficacy of anti-PD1 therapy in pancreatic ductal adenocarcinoma
Liu, J., Jiang, W., Zhao, K., Wang, H., Zhou, T., Bai, W., Wang, X., Zhao, T., Huang, C., Gao, S., et al. (2019) · The Journal of Experimental Medicine · doi:10.1084/jem.20180749 · Cited by 53
Xu, Y., Fang, F., Jiao, H., Zheng, X., Huang, L., Yi, X., & Zhao, W. (2019) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-019-02414-9 · Cited by 53
Primary and acquired resistance mechanisms to immune checkpoint inhibition in Hodgkin lymphoma
Veldman, J., Visser, L., van den Berg, A., & Diepstra, A. (2019) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2019.101931 · Cited by 53
“Recruitment of suppressive cell populations [21,22]”
Alvarez-Breckenridge, C. A., Markson, S. C., Stocking, J. H., Nayyar, N., Lastrapes, M., Strickland, M. R., Kim, A. E., de Sauvage, M. A., Dahal, A., Larson, J. M., et al. (2022) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-21-0870 · Cited by 55
Cancer cell-derived type I interferons instruct tumor monocyte polarization
Kwart, D., He, J., Srivatsan, S., Lett, C., Golubov, J., Oswald, E. M., Poon, P., Ye, X., Waite, J. C., Zaretsky, A. G., et al. (2022) · Cell Reports · doi:10.1016/j.celrep.2022.111769 · Cited by 53
Targeting KRAS mutations: orchestrating cancer evolution and therapeutic challenges
Choucair, K., Imtiaz, H., Uddin, M. H., Nagasaka, M., Al-Hallak, M. N., Philip, P. A., El-Rayes, B., Pasche, B., & Azmi, A. S. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02473-8 · Cited by 67
“301,302 Other combinations of SHP2, KRAS, and IC inhibitors may also reshape the TME and suppress the adaptive signaling of cancer cells, which diminishes sensitivity to KRAS G12C inhibition.”
Hu‐Lieskovan, S., & Ribas, A. (2017) · The Cancer Journal · doi:10.1097/ppo.0000000000000246 · Cited by 52
“In a mouse model of breast cancer, combination of a CCR1 inhibitor (CCX9588) and PD-L1 inhibitor synergistically reduced the tumor burden,(185) and anti-CXCR2 plus anti–PD-1 improved survival in a rhabdomyosarcoma model.(184) CCR4 is highly expressed by Tregs in the blood and tumors,(186) and anti-CCR4 inhibits Treg r…”
BackgroundThe Role of Myeloid-Derived Suppressor Cells in Viral Infection
O’Connor, M. A., Rastad, J. L., & Green, W. R. (2017) · Viral Immunology · doi:10.1089/vim.2016.0125 · Cited by 51
“Murine and human MDSCs may also express different combinations of chemokine receptors needed for egress of MDSCs out of the bone marrow and/or migration to tumor sites or sites of infection, such as CCR2, CXCR4, CXCR2, and/or CX3CR1 (9,58,62,68,86,111,112,133,138,173,176).”
Versatile neutrophil functions in cancer
Siwicki, M. R., & Pittet, M. J. (2021) · Seminars in Immunology · doi:10.1016/j.smim.2021.101538 · Cited by 52
Azeez, S. S., Yashooa, R. K., Smail, S., Salihi, A., Ali, A. S., Mamand, S., & Janson, C. (2025) · Molecular Cancer · doi:10.1186/s12943-025-02386-8 · Cited by 56
Targeting Myeloid Cells in Combination Treatments for Glioma and Other Tumors
Ding, A. S., Routkevitch, D., Jackson, C., & Lim, M. K. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01715 · Cited by 51
The Current Landscape of Antibody-based Therapies in Solid Malignancies
Shah, A., Rauth, S., Aithal, A., Kaur, S., Ganguly, K., Orzechowski, C., Varshney, G. C., Jain, M., & Batra, S. K. (2020) · Theranostics · doi:10.7150/thno.52614 · Cited by 54
“CXCR2 inhibition in combination with ICB antibodies Inhibit trafficking of MDSCs to tumor site Pediatric sarcomas [69]”
BackgroundMechanisms of drug resistance to immune checkpoint inhibitors in non-small cell lung cancer
Zhou, K., Li, S., Zhao, Y., & Cheng, K. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1127071 · Cited by 49
Ledo, A. M., Sasso, M. S., Bronte, V., Marigo, I., Boyd, B. J., García-Fuentes, M., & Alonso, M. J. (2018) · Journal of Controlled Release · doi:10.1016/j.jconrel.2018.12.041 · Cited by 49
Neutrophil metabolism in the cancer context
Bodac, A., & Meylan, E. (2021) · Seminars in Immunology · doi:10.1016/j.smim.2021.101583 · Cited by 50
“myosarcoma, inhibition of CXCR2-dependent neutrophil trafficking enhanced the effect of anti-PD1 blockade [43].”
BackgroundResistance to immune checkpoint inhibitors and the tumor microenvironment
Kawashima, S., & Togashi, Y. (2022) · Experimental Dermatology · doi:10.1111/exd.14716 · Cited by 50
Conditioning solid tumor microenvironment through inflammatory chemokines and S100 family proteins
Nasser, M. W., Elbaz, M., Ahirwar, D. K., & Ganju, R. K. (2015) · Cancer Letters · doi:10.1016/j.canlet.2015.05.002 · Cited by 48
Therapeutic prospects of targeting myeloid‐derived suppressor cells and immune checkpoints in cancer
Toor, S. M., & Elkord, E. (2018) · Immunology and Cell Biology · doi:10.1111/imcb.12054 · Cited by 48
“Inhibition of CXCR2 G-MDSC trafficking to the TME by CXCR2 targeting with anti-CXCR2 monoclonal antibody in murine rhabdomyosarcoma model improved anti-PD-1 treatment.(66) Moreover, expansion of G-MDSC correlated with reduced effector immune cell infiltration in head and neck cancer tumor model, while selective deplet…”
MethodKather, J. N., Hörner, C., Weis, C., Aung, T., Vokuhl, C., Weiß, C., Scheer, M., Marx, A., & Simon‐Keller, K. (2019) · Scientific Reports · doi:10.1038/s41598-019-45551-y · Cited by 49
Myeloid-derived suppressor cells are necessary for development of pulmonary hypertension
Bryant, A. J., Shenoy, V., Fu, C., Marek, G., Lorentsen, K. J., Herzog, E. L., Brantly, M. L., Avram, D., & Scott, E. W. (2018) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2017-0214oc · Cited by 47
Giannotta, C., Autino, F., & Massaia, M. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1102471 · Cited by 50
“Lastly, CXCR2 is another cell surface molecule that is critical in mice models and paediatric sarcoma to promote the accumulation of MDSC in the TME and hamper the efficacy of anti-PD-1 treatment (28).”
BackgroundTherapeutic Targets and Emerging Treatments in Advanced Chondrosarcoma
Miwa, S., Yamamoto, N., Hayashi, K., Takeuchi, A., Igarashi, K., & Tsuchiya, H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23031096 · Cited by 48
Targeting the Tumor Microenvironment: A Close Up of Tumor-Associated Macrophages and Neutrophils
Russo, M., & Nastasi, C. (2022) · Frontiers in Oncology · doi:10.3389/fonc.2022.871513 · Cited by 45
“In fact, the inhibition of CXCR2 in a murine model of a soft tissue sarcoma resistant to anti-PD1 treatment restored the effectiveness of the immunotherapy (81).”
Background
Metadata
- Authors
- Highfill, S. L., Cui, Y., Giles, A. J., Smith, J. P., Zhang, H., Morse, E., Kaplan, R. N., & Mackall, C. L.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Mackall, Crystal L.
- Venue
- Science Translational Medicine
- Published
- 2014-05-21
- Volume
- 6
- Issue
- 237
- Pages
- 237ra67-237ra67
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6980372
- OpenAlex
- W2171524684
- Cited by
- 767
- References
- 50
- Citations by year
- 2026: 55 · 2025: 62 · 2024: 57 · 2023: 83 · 2022: 73 · 2021: 100 · 2020: 91 · 2019: 60 · 2018: 52 · 2017: 52 · 2016: 38 · 2015: 31 · 2014: 12
- FWCI
- 20.24
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (Z01BC011072, Z01BC010566, Z01SC010289)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- CXCR2, myeloid-derived suppressor cells, tumor immune evasion, anti-PD-1 therapy, rhabdomyosarcoma, pediatric sarcoma, interleukin-8, PD-L1, tumor immunosuppression
- MeSH terms
- Adolescent, Adult, Animals, Antibodies, Monoclonal, Antigens, Ly, Antineoplastic Combined Chemotherapy Protocols, Chemotaxis, Child, Child, Preschool, Female, Humans, Male, Mice, Inbred C57BL, Prognosis, Rhabdomyosarcoma, Time Factors, Neoplastic Stem Cells, Case-Control Studies, Cytokines, Interleukin-8, Mice, Knockout, Tumor Escape, Receptors, Interleukin-8B, CD11b Antigen, Cell Line, Tumor, Tumor Burden, Mice, Chemokine CXCL1, Young Adult, Tumor Microenvironment, B7-H1 Antigen
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