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Publication : Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice.

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.
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