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Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice
Author(s) -
Reiko Shinkura,
Fumihiko Matsuda,
Toshio Sakiyama,
Takeshi Tsubata,
Hiroshi Hial,
Michael Paumen,
Shigeki Miyawaki,
Tasuku Honjo
Publication year - 1996
Publication title -
international immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.86
H-Index - 134
eISSN - 1460-2377
pISSN - 0953-8178
DOI - 10.1093/intimm/8.7.1067
Subject(s) - somatic hypermutation , germinal center , immunoglobulin class switching , affinity maturation , spleen , biology , isotype , b cell , somatic cell , immunology , lymph , germline mutation , antibody , mutant , mutation , microbiology and biotechnology , genetics , monoclonal antibody , pathology , medicine , gene
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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