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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.

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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.
University of Chinese Academy of Sciences, Beijing 100049, China.
Medical Department for Gastroenterology, Infectious Diseases and Rheumatology/Research Center ImmunoSciences, Campus Benjamin Franklin, Charité-Universitätsmedizin Berlin, Berlin 12200, Germany.
Infinitus Chinese Herbal Immunity Research Centre, Guangzhou 510665, China.
Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine Berlin-Buch, Berlin 13125, Germany.


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.

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