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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Bibliographic Details
Published in:Journal for immunotherapy of cancer Vol. 4; no. 1; p. 40
Main Authors: Schwartz, Marc, Zhang, Yu, Rosenblatt, Joseph D.
Format: Journal Article
Language:English
Published: London BMJ Publishing Group Ltd 19.07.2016
BioMed Central
BioMed Central Ltd
BMJ Publishing Group LTD
BMJ Publishing Group
Subjects:
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
Online Access:Get full text
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Summary: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.
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ISSN:2051-1426
2051-1426
DOI:10.1186/s40425-016-0145-x