Journal
CANCER IMMUNOLOGY IMMUNOTHERAPY
Volume 67, Issue 12, Pages 1949-1953Publisher
SPRINGER
DOI: 10.1007/s00262-018-2245-6
Keywords
CCR5; Mobilization; Colonization; MDSC; Cancer; CITIM 2017
Categories
Funding
- Israel Science Foundation (ISF) [630/15] Funding Source: Medline
- Israel Cancer Research Fund (US) (ICRF) [171961-PG] Funding Source: Medline
- The co-operational research program of the DKFZ, Heidelberg, Germany, with the Ministry of Science, Technology & Space of Israel fund in cancer research (DKFZ-MOST) [CA157] Funding Source: Medline
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Bone marrow (BM) cells of the hematopoietic system, also known as BM-derived leukocytes (BMD), are mobilized from the BM to the blood and then colonize tumor sites. These cells then become key players in either promoting or regulating the development and progression of tumors. Among the cells that suppress anti-tumor immunity are regulatory T cells (T-regs), tumor-associated macrophages (TAMS) and myeloid-derived suppressor cells (MDSC). MDSC comprise CD11b(+)Gr1(+)Ly6C(low) polymorphonuclear myeloid cells (PMN-MDSC), and CD11b(+)Gr1(+)Ly6C(high) monocytic myeloid cells (Mo-MDSC). Several studies including ours have identified the CCR2-CCL2 axis as the key driver of the mobilization of monocytic cells from the BM to the blood and later their colonization at the tumor site. The current review focuses on the mechanisms by which PMN-MDSC are mobilized from the BM to the blood and later to the tumor site, and their clinical implications.
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