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

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, albelt weakly, to either T cell-dependent or T cell-Independent antigen by aly/aly mutants. Howe...

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Bibliographic Details
Published in:International immunology 1996-07, Vol.8 (7), p.1067-1075
Main Authors: Shinkura, Reiko, Matsuda, Fumihiko, Sakiyama, Toshio, Tsubata, Takeshi, Hial, Hiroshi, Paumen, Michael, Miyawaki, Shigeki, Honjo, Tasuku
Format: Article
Language:English
Subjects:
aly/aly mice
Amino Acid Sequence
Animals
Antibody Formation - genetics
Antibody Specificity
Antigens, T-Independent - physiology
Base Sequence
Genetic Variation - genetics
Genetic Variation - immunology
Germinal Center - pathology
immune response
Immunoglobulin Class Switching
Immunologic Deficiency Syndromes - genetics
Immunologic Deficiency Syndromes - pathology
Lymph Nodes - abnormalities
Lymphoid Tissue - abnormalities
Mice
Mice, Mutant Strains
Molecular Sequence Data
Mutation - immunology
Peyer's Patches - abnormalities
somatic hypermutation
Spleen - abnormalities
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Summary: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, albelt 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.
ISSN:0953-8178
1460-2377
DOI:10.1093/intimm/8.7.1067