期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 37, 期 2, 页码 358-367出版社
WILEY
DOI: 10.1002/eji.200636453
关键词
B cells; cell differentiation; cell surface; molecules; toll-like receptors
类别
It is becoming increasingly clear that the regulation of proliferation and differentiation of B cells to plasma cells involves the integration of a variety of intracellular signals provided by receptors of both the adaptive and innate immune system. The cross-linking of the surface molecule CD38 induces calcium mobilization, protein phosphorylation and NF-kappa B translocation into the nucleus, ultimately leading to proliferation and isotype switching toward IgG1. Here we describe (a) the effect on B cell activation of stimulating through both CD38 and Toll-like receptors 4, 7 and 9; and (b) that CD38 cross-linking increases the number of proliferating cells and the rate of proliferation in LPS-stimulated B cells by a Bruton's tyrosine kinase- and protein kinase C-dependent mechanism. In contrast, CD38 cross-linking reduces the number of cells committed to IgM plasma cell differentiation as measured by the number of CD138(+) cells, antibody secretion, and the expression of PAX5, Bcl6 and Blimp-1. Since a putative ligand for CD38 is expressed by germinal center follicular dendritic cells, and CD38 expression is down-regulated in germinal center B cells, we speculate that CD38 might participate in the outcome of post-germinal center antibody responses.
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