| First Author | Faust KB | Year | 2007 |
| Journal | Clin Exp Immunol | Volume | 150 |
| Issue | 1 | Pages | 132-9 |
| PubMed ID | 17645767 | Mgi Jnum | J:125271 |
| Mgi Id | MGI:3758113 | Doi | 10.1111/j.1365-2249.2007.03456.x |
| Citation | Faust KB, et al. (2007) Antigen-induced B cell apoptosis is independent of complement C4. Clin Exp Immunol 150(1):132-9 |
| abstractText | Deficiencies in early complement components are associated with the development of systemic lupus erythematosus (SLE) and therefore early complement components have been proposed to influence B lymphocyte activation and tolerance induction. A defect in apoptosis is a potential mechanism for breaking of peripheral B cell tolerance, and we hypothesized that the lack of the early complement component C4 could initiate autoimmunity through a defect in peripheral B lymphocyte apoptosis. Previous studies have shown that injection of a high dose of soluble antigen, during an established primary immune response, induces massive apoptotic death in germinal centre B cells. Here, we tested if the antigen-induced apoptosis within germinal centres is influenced by early complement components by comparing complement C4-deficient mice with C57BL/6 wild-type mice. We demonstrate that after the application of a high dose of soluble antigen in wild-type mice, antibody levels declined temporarily but were restored almost completely after a week. However, after antigen-induced apoptosis, B cell memory was severely limited. Interestingly, no difference was observed between wild-type and complement C4-deficient animals in the number of apoptotic cells, restoration of antibody levels and memory response. |
