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Int Immunol. 1996 Jul;8(7):1067-75.

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

Author information

1
Department of Medical Chemistry, Center for Molecular Biology and Genetics, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606, Japan.

Abstract

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.

PMID:
8757952
DOI:
10.1093/intimm/8.7.1067
[Indexed for MEDLINE]

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