| First Author | Smith KG | Year | 1995 |
| Journal | Proc Natl Acad Sci U S A | Volume | 92 |
| Issue | 25 | Pages | 11628-32 |
| PubMed ID | 8524817 | Mgi Jnum | J:30157 |
| Mgi Id | MGI:77671 | Doi | 10.1073/pnas.92.25.11628 |
| Citation | Smith KG, et al. (1995) FAS is highly expressed in the germinal center but is not required for regulation of the B-cell response to antigen. Proc Natl Acad Sci U S A 92(25):11628-32 |
| abstractText | In establishing the memory B-cell population and maintaining self-tolerance during an immune response, apoptosis mediates the removal of early, low-affinity antibody-forming cells, unselected germinal center (GC) cells, and, potentially, self-reactive B cells. To address the role of the apoptosis-signaling cell surface molecule FAS in the B-cell response to antigen, we have examined the T-cell-dependent B-cell response to the carrier-conjugated hapten (4-hydroxy-3-nitrophenyl)acetyl (NP) in lpr mice in which the fas gene is mutated. High levels of FAS were expressed on normal GC B cells but the absence of FAS did not perturb the progressive decline in numbers of either GC B cells or extrafollicular antibody-forming cells. Furthermore, the rate of formation and eventual size of the NP-specific memory B-cell population in lpr mice were normal. The accumulation of cells with affinity-enhancing mutations and the appearance of high-affinity anti-NP IgG1 antibody in the serum were also normal in lpr mice. Thus, although high levels of FAS are expressed on GC B cells, FAS is not required for GC selection or for regulation of the major antigen-specific B-cell compartments. The results suggest that the size and composition of B-cell compartments in the humoral immune response are regulated by mechanisms that do not require FAS. |
