H-2-linked control of cytotoxic T-cell responsiveness to alphavirus infection. Presence of H-2Dk during differentiation and stimulation converts stem cells of low responder genotype to T cells of responder phenotype.
Secondary Tc cells generated against Sindbis virus (SIN) are restricted to Dk. All other H-2K or D regions tested show low specific responsiveness. F1 hybrids between low and high responders show dominance of responsiveness but lack complementation. When BALB/c (KdIdDd) low responder fetal liver stem cells were allowed to mature in irradiated high responder recipients C3H.OH (KdIdDk) a response to Dk plus SIN could be generated with Tc cells of BALB/c origin. This result, together with the failure of complementation in the F1 hybrids, implies that the lesion of low responsiveness is in the inability of viral antigen to stimulate a Tc-cell response in association with any self H-2K or H-2D molecule (of those tested) other than H-2Dk. Hypotheses compatible with these data are discussed.
D000818:Animals; D001102:Arbovirus Infections / Q000276:immunology*; D002454:Cell Differentiation; D003602:Cytotoxicity, Immunologic; D005260:Female; D005802:Genes, MHC Class II; D008040:Genetic Linkage; D006183:H-2 Antigens / Q000235:genetics*; D006412:Hematopoietic Stem Cells / Q000166:cytology; D007156:Immunologic Memory; D051379:Mice; D012845:Sindbis Virus / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D006183:H-2 Antigens