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Transcriptional regulation of natural IgM secretion by a novel B‐1 cell population in the bone marrow
Author(s) -
CHOI YOUN SOO,
BAUMGARTH NICOLE
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.847.9
Subject(s) - b 1 cell , b cell , bone marrow , microbiology and biotechnology , population , biology , spleen , naive b cell , secretion , antibody , antigen , cd40 , immunology , chemistry , antigen presenting cell , immune system , t cell , cytotoxic t cell , medicine , endocrinology , genetics , in vitro , environmental health
B‐1 cells are an important source for much of the polyreactive natural antibodies (Ab) that are secreted in the absence of antigenic challenge to protect against pathogens. However, the molecular pathways underlying their differentiation to Ab‐secreting cells are incompletely understood. Contradictory data exist as to whether the transcriptional regulators that control differentiation of conventional B cells to Ab‐generating plasma cells (paired box protein 5a (PAX‐5a), B lymphocyte induced maturation protein 1 (BLIMP‐1), and X‐box binding protein 1 (XBP‐1)) also control B‐1 cell differentiation. Using Ig‐allotype chimeric mice, in which B‐1 cells and their Abs are distinguished from conventional B cells, we identified a novel IgM‐secreting B‐1 cell population in the bone marrow (BM). Together with splenic B‐1 cells, these cells are the major source of natural IgM. While B‐1 cells are abundant in the peritoneal cavity (PerC), there they secrete little IgM. Intracytoplasmic staining and qRT‐PCR analysis of FACS‐purified B‐1 cells from BM, spleen and PerC revealed a clear correlation between high levels of expression for BLIMP‐1, XBP‐1 and sXBP‐1 and the ability of B‐1 cells to secrete IgM. In contrast to conventional B cells, however, B‐1 cells retained high levels of PAX‐5a. The data point to novel regulatory pathways controlling differentiation of natural IgM‐secreting B‐1 cells. This work was supported by NIH/NIAID AI051354.