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Cell Mol Immunol. 2017 Jul;14(7):597-606. doi: 10.1038/cmi.2015.103. Epub 2016 May 2.

Myeloid-derived suppressor cells promote B-cell production of IgA in a TNFR2-dependent manner.

Author information

1
Key Laboratory of Protein and Peptide Pharmaceuticals, Chinese Academy of Sciences-University of Tokyo Joint Laboratory of Structural Virology and Immunology, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
2
University of Chinese Academy of Sciences, Beijing 100049, China.
3
Medical Department for Gastroenterology, Infectious Diseases and Rheumatology/Research Center ImmunoSciences, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin 12200, Germany.
4
Infinitus Chinese Herbal Immunity Research Centre, Guangzhou 510665, China.
5
Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine Berlin-Buch, Berlin 13125, Germany.

Abstract

Myeloid-derived suppressor cells (MDSCs) are well known for their capacity to suppress antitumor T-cell responses, but their effects on B-cell function and antibody production remain unclear. Here, we found that MDSCs that accumulated around the germinal center in the spleen of tumor-bearing mice co-located with B cells. In the presence of MDSCs, the antibody reaction to a surrogate antigen was significantly enhanced in mice, especially the immunoglobulin (Ig)A subtype. Co-culture with MDSCs promoted both proliferation and differentiation of B cells into IgA-producing plasma cells in vitro. Interestingly, the cross talk between MDSCs and B cells required cell-cell contact. MDSCs from tumor necrosis factor receptor (TNFR) 2-/- mice, but not from TNFR1-/- mice, failed to promote B-cell responses. Further investigation suggested that interleukin-10 and transforming growth factor-β1 were crucial for the MDSC-mediated promotion of IgA responses. These results demonstrate a novel mechanism of MDSC-mediated immune regulation during tumor growth.

PMID:
27133471
PMCID:
PMC5520412
DOI:
10.1038/cmi.2015.103
[Indexed for MEDLINE]
Free PMC Article

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