First Author | Shinkura R | Year | 1996 |
Journal | Int Immunol | Volume | 8 |
Issue | 7 | Pages | 1067-75 |
PubMed ID | 8757952 | Mgi Jnum | J:34300 |
Mgi Id | MGI:81760 | Doi | 10.1093/intimm/8.7.1067 |
Citation | Shinkura R, et al. (1996) Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice. Int Immunol 8(7):1067-75 |
abstractText | The alymphoplasia (aly) mutation of mice causes the systemic absence of lymph nodes, Peyer's patches and well- defined lymphoid follicles in the spleen. We found that antibody responses are elicited, albeit weakly, to either T cell-dependent or T cell-independent antigen by aly/aly mutants. However, isotype switching was defective. The T cell-dependent immune response was not elicited in splenectomized aly/aly mice. Neither hypermutation nor germinal center formation was observed in aly/aly mice. These results suggest that T-B collaboration requires either lymph nodes or spleen, and that hypermutation and affinity maturation depend on germinal center formation. |