title: Gain/loss of poly(Glu50Tyr50)/poly(Glu60Ala30Tyr10) responsiveness in the bm12 mutant strain.
abstract: The development of inbred strains of mutant mice has proven useful in ascribing specific gene functions to particular genetic loci within the regions and subregions of the H-2 complex. The B6.C-H-2bm12 (bm12) strain is of particular interest in that, compared to parental C57Bl/6Kh (B6) mice, it bears a presumptive single gene mutation altering the Ab beta chain encoded by the I-A subregion. Our data show that bm12 mice have gained the ability to respond to poly(Glu50Tyr50)(GT) and have lost the ability to make plaque-forming cell or delayed-type hypersensitivity responses to the closely related copolymer, poly(Glu60Ala30Tyr10)(GAT), although retaining the ability to mount a GAT-specific T cell proliferative response. This is in sharp contrast to the parental B6 strain, which is a GT nonresponder and a GAT responder. Thus, this study is the first to report the establishment of responder status as a consequence of mutation. Possible mechanisms accounting for the gain/loss of GT/GAT responsiveness in the context of a two-step helper T cell model are discussed.
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D006183:H-2 Antigens / Q000235:genetics*; D006462:Hemolytic Plaque Technique; D006968:Hypersensitivity, Delayed; D007166:Immunosuppressive Agents / Q000276:immunology*; D036341:Intercellular Signaling Peptides and Proteins; D008214:Lymphocytes / Q000276:immunology*; D008285:Major Histocompatibility Complex; D051379:Mice; D008807:Mice, Inbred BALB C; D008815:Mice, Inbred Strains; D009154:Mutation; D010455:Peptides / Q000276:immunology*; D011108:Polymers; D013045:Species Specificity; D013154:Spleen / Q000276:immunology
chemical_list: D006183:H-2 Antigens; D007166:Immunosuppressive Agents; D036341:Intercellular Signaling Peptides and Proteins; D010455:Peptides; D011108:Polymers; C020749:GAT; C027606:L-glutamic acid-L-tyrosine copolymer