Ir gene control of the cytotoxic T lymphocyte response to Sendai virus: H-2k mice are low responders to Sendai.
H-2k mice generate a secondary in vitro cytotoxic T lymphocyte response to Sendai virus 20- to 100-fold weaker than those of other haplotypes tested (H-2b,d,q,s). This immune response defect maps to both H-2K and H-2D. H-2k x H-2d F1 mice (responder x nonresponder) only lyse targets that have the d allele at H-2K and/or H-2D. H-2k targets are equally lysable with anti-Sendai antibody. Furthermore, H-2k mice demonstrate normal antibody and T cell proliferation responses to Sendai virus. The Ir gene defect therefore appears to be limited to the generation of the cytotoxic T lymphocytes.
D000818:Animals; D000914:Antibodies, Viral / Q000096:biosynthesis; D002874:Chromosome Mapping; D003602:Cytotoxicity, Immunologic; D004306:Dose-Response Relationship, Immunologic; D005802:Genes, MHC Class II; D006183:H-2 Antigens; D007153:Immunologic Deficiency Syndromes / Q000235:genetics; D008213:Lymphocyte Activation; D051379:Mice; D008805:Mice, Inbred A; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D010222:Parainfluenza Virus 1, Human / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
D000914:Antibodies, Viral; D006183:H-2 Antigens