Journal
IMMUNOTHERAPY
Volume 4, Issue 3, Pages 291-304Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/IMT.11.178
Keywords
APC; arginase 1; immune suppression; immune therapy; lung cancer; myeloid-derived suppressor cells; nitric oxide synthase; T lymphocytes; tumor genetic signature
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Funding
- NCI NIH HHS [R01 CA126944-05, R01 CA126944] Funding Source: Medline
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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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