| First Author | Manjarrez-Orduño N | Year | 2007 |
| Journal | Eur J Immunol | Volume | 37 |
| Issue | 2 | Pages | 358-67 |
| PubMed ID | 17274001 | Mgi Jnum | J:117900 |
| Mgi Id | MGI:3697967 | Doi | 10.1002/eji.200636453 |
| Citation | Manjarrez-Orduno N, et al. (2007) CD38 cross-linking enhances TLR-induced B cell proliferation but decreases IgM plasma cell differentiation. Eur J Immunol 37(2):358-67 |
| abstractText | 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-kappaB 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. |
