B cell regulation of the anti-tumor response and role in carcinogenesis

The balance between immune effector cells such as T cells and natural killer cells, and immunosuppressive Treg cells, dendritic, myeloid and monocytic sub-populations in the tumor microenvironment acts to calibrate the immune response to malignant cells. Accumulating evidence is pointing to a role f...

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Vydáno v:	Journal for immunotherapy of cancer Ročník 4; číslo 1; s. 40
Hlavní autoři:	Schwartz, Marc, Zhang, Yu, Rosenblatt, Joseph D.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London BMJ Publishing Group Ltd 19.07.2016 BioMed Central BioMed Central Ltd BMJ Publishing Group LTD BMJ Publishing Group
Témata:	Analysis Anti-tumor immunity Apoptosis Arthritis B cells B regulatory cells Blood cancer Cancer Carcinogenesis Cell growth Cytokines Immune response Immunology Immunotherapy Inflammatory bowel disease Ligands Liver cancer Lung cancer Lymphocytes Lymphoma Medicine Medicine & Public Health Metastasis Oncology Ovaries Review Reviews T cell receptors Tumor necrosis factor-TNF Tumors B regulatory cells Carcinogenesis Anti-tumor immunity
ISSN:	2051-1426, 2051-1426
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Popis
Shrnutí:	The balance between immune effector cells such as T cells and natural killer cells, and immunosuppressive Treg cells, dendritic, myeloid and monocytic sub-populations in the tumor microenvironment acts to calibrate the immune response to malignant cells. Accumulating evidence is pointing to a role for B cells in modulating the immune response to both solid tumors and hematologic cancer. Evidence from murine autoimmune models has defined B regulatory cell (Breg) subsets that express cytokines such as IL-10, TGF-β, and/or express immune regulatory ligands such as PD-L1, which can suppress T cell and/or natural killer cell responses. Multiple murine tumor models exhibit decreased tumor growth in B cell deficient or B cell depleted mice. In several of these models, B cells inhibit T cell mediated tumor immunity and/or facilitate conversion of T cells to CD4+CD25+FoxP3+ T regs, which act to attenuate the innate and/or adaptive antitumor immune response.Mechanisms of suppression include the acquisition of inhibitory ligand expression, and phosphorylation of Stat3, and induction of IL-10 and TGF-β, resulting in a Breg phenotype. Breg suppressive activity may affect diverse cell subtypes, including T effector cells, NK cells, myeloid derived suppressor cells (MDSC) and/or tumor associated macrophages. B cells may also directly promote tumorigenesis through recruitment of inflammatory cells, and upregulation of pro-angiogenic genes and pro-metastatic collagenases.Breg infiltration has now been identified in a variety of solid tumor malignancies including but not limited to ovarian, gastric, non-small cell lung cancer, pancreatic, esophageal, head and neck, and hepatocellular carcinomas. Increasing evidence suggests that recruitment of B cells and acquisition of suppressive activity within the tumor bed may be an important mechanism through which B cells may modulate innate and/or adaptive anti-tumor immunity. B cell depletion in the clinic using anti-CD20 antibodies and/or inhibitors of BTK and/or other signaling pathways, may be a useful strategy for augmenting the anti-tumor immune response.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23
ISSN:	2051-1426 2051-1426
DOI:	10.1186/s40425-016-0145-x