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

Int Immunol. 1996 Jul;8(7):1067-75. doi: 10.1093/intimm/8.7.1067.

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.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Antibody Formation / genetics
  • Antibody Specificity
  • Antigens, T-Independent / physiology
  • Base Sequence
  • Genetic Variation / genetics
  • Genetic Variation / immunology
  • Germinal Center / pathology
  • 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
  • Spleen / abnormalities

Substances

  • Antigens, T-Independent