title: Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice.
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.
authors: Department of Medical Chemistry, Center for Molecular Biology and Genetics, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606, Japan.
authors: R
authors: R
authors: Shinkura
authors: F
authors: F
authors: Matsuda
authors: T
authors: T
authors: Sakiyama
authors: T
authors: T
authors: Tsubata
authors: H
authors: H
authors: Hiai
authors: M
authors: M
authors: Paumen
authors: S
authors: S
authors: Miyawaki
authors: T
authors: T
authors: Honjo
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D000917:Antibody Formation / Q000235:genetics; D000918:Antibody Specificity; D000955:Antigens, T-Independent / Q000502:physiology; D001483:Base Sequence; D014644:Genetic Variation / Q000235:genetics / Q000276:immunology; D018858:Germinal Center / Q000473:pathology; D017578:Immunoglobulin Class Switching; D007153:Immunologic Deficiency Syndromes / Q000235:genetics* / Q000473:pathology; D008198:Lymph Nodes / Q000002:abnormalities; D008221:Lymphoid Tissue / Q000002:abnormalities*; D051379:Mice; D008817:Mice, Mutant Strains; D008969:Molecular Sequence Data; D009154:Mutation / Q000276:immunology*; D010581:Peyer's Patches / Q000002:abnormalities; D013154:Spleen / Q000002:abnormalities
chemical_list: D000955:Antigens, T-Independent