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Myeloid suppressor cells and immune modulation in lung cancer

期刊

IMMUNOTHERAPY
卷 4, 期 3, 页码 291-304

出版社

FUTURE MEDICINE LTD
DOI: 10.2217/IMT.11.178

关键词

APC; arginase 1; immune suppression; immune therapy; lung cancer; myeloid-derived suppressor cells; nitric oxide synthase; T lymphocytes; tumor genetic signature

资金

  1. NCI NIH HHS [R01 CA126944-05, R01 CA126944] Funding Source: Medline

向作者/读者索取更多资源

Many tumors, including lung cancers, promote immune tolerance to escape host immune surveillance and facilitate tumor growth. Tumors utilize numerous pathways to inhibit immune responses, including the elaboration of immune-suppressive mediators such as PGE2, TGF-beta, IL-10, VEGF, GM-CSF, IL-6, S100A8/A9 and SCF, which recruit and/or activate myeloid-derived suppressor cells (MDSCs). MDSCs, a subset of heterogeneous bone marrow-derived hematopoietic cells, are found in the peripheral blood of cancer patients and positively correlate to malignancy. Solid tumors contain MDSCs that maintain an immune-suppressive network in the tumor microenvironment. This review will focus on the interaction of tumors with MDSCs that lead to dysregulation of antigen presentation and T-cell activities in murine tumor models. Specific genetic signatures in lung cancer modulate the activities of MDSCs and impact tumor progression. Targeting MDSCs may have a long-term antitumor benefit and is at the forefront of anticancer therapeutic strategies.

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