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Mouse IgM Fc Receptor, FCMR, Promotes B Cell Development and Modulates Antigen-Driven Immune Responses
Author(s) -
SeungChul Choi,
Hongsheng Wang,
Linjie Tian,
Yousuke Murakami,
DongMi Shin,
Francisco Borrego,
Herbert C. Morse,
John E. Coligan
Publication year - 2012
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1202227
Subject(s) - germinal center , b cell , b 1 cell , biology , naive b cell , immunology , b cell receptor , autoimmunity , immune system , antigen , cd40 , microbiology and biotechnology , plasma cell , autoantibody , antibody , t cell , antigen presenting cell , cytotoxic t cell , in vitro , biochemistry
FcR specific for pentameric IgM (FCMR) is expressed at high levels by B cells. Although circulating IgM has profound effects on responses to pathogens, autoimmunity, and B cell homeostasis, the biologic consequences of its binding to FCMR are poorly understood. We interrogated FCMR contributions to B cell function by studying mice that lack FCMR. FCMR transcripts are expressed at different levels by various B cell subsets. FCMR-deficient mice have reduced numbers of developing B cells, splenic follicular and peritoneal B-2 cells, but increased levels of peritoneal B-1a cells and autoantibodies. After immunization, germinal center B cell and plasma cell numbers are increased. FCMR-deficient B cells are sensitive to apoptosis induced by BCR ligation. Our studies demonstrate that FCMR is required for B cell differentiation and homeostasis, the prevention of autoreactive B cells, and responsiveness to antigenic challenge.

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