Myeloid-derived suppressor cells promote B-cell production of IgA in a TNFR2-dependent manner
作者机构:Key Laboratory of Protein and Peptide PharmaceuticalsChinese Academy of Sciences-University of Tokyo Joint Laboratory of Structural Virology and ImmunologyInstitute of BiophysicsChinese Academy of SciencesBeijing 100101China University of Chinese Academy of SciencesBeijing 100049China Medical Department for GastroenterologyInfectious Diseases and Rheumatology/Research Center ImmunoSciencesCampus Benjamin FranklinCharité-Universitätsmedizin BerlinBerlin 12200Germany Infinitus Chinese Herbal Immunity Research CentreGuangzhou 510665China Berlin Institute for Medical Systems BiologyMax Delbrück Center for Molecular Medicine Berlin-BuchBerlin 13125Germany
出 版 物:《Cellular & Molecular Immunology》 (中国免疫学杂志(英文版))
年 卷 期:2017年第14卷第7期
页 面:597-606页
核心收录:
学科分类:0710[理学-生物学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100214[医学-肿瘤学] 10[医学]
基 金:supported by the Ministry of Science and Technology of China(2012CB917103,2012CB934003) the National Natural Science Foundation of China(91229203) the German Research Foundation(DFG 749-6/1 and SFB 633)
摘 要: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 ***,we found that MDSCs that accumulated around the germinal center in the spleen of tumor-bearing mice co-located with B *** the presence of MDSCs,the antibody reaction to a surrogate antigen was significantly enhanced in mice,especially the immunoglobulin(Ig)A ***-culture with MDSCs promoted both proliferation and differentiation of B cells into IgA-producing plasma cells in ***,the cross talk between MDSCs and B cells required cell-cell *** from tumor necrosis factor receptor(TNFR)2^(−/−)mice,but not from TNFR1^(−/−)mice,failed to promote B-cell *** investigation suggested that interleukin-10 and transforming growth factor-β1 were crucial for the MDSC-mediated promotion of IgA *** results demonstrate a novel mechanism of MDSC-mediated immune regulation during tumor growth.