Cellular and genetic control of antibody responses in vitro. II. Ir gene control of primary IgM responses to trinitrophenyl conjugates of poly-L-(Tyr,Glu)-poly-D,L-Ala--poly-L-Lys and poly-L-(His,Glu)-poly-D,L-Ala--poly-L-Lys.
The in vitro primary IgM anti-hapten responses to trinitrophenyl (TNP) conjugates of poly-L-(Tyr,Glu)-poly-D,L-Ala-poly-L-Lys (T,G)-A--L and poly-L(His,Glu)-poly-D,L-Ala--poly-L-Lys (H,G)-A--L were shown to be T-cell dependent and under autosomal dominant H-2-linked Ir gene control which mapped within the K or I-A regions of the H-2 complex. The in vitro response to TNP-keyhole limpet hemocyanin, while T-dependent, was not under demonstrable genetic control. The genes governing the in vitro primary IgM anti-hapten responses to TNP-(T,G)-A--L and TNP-(H,G)-A--L resemble the Ir genes controlling the in vivo secondary IgG responses to (T,G)-A--L and (H,G)-A--L in that they are autosomal dominant, map identically within the H-2 complex, and have identical responder and nonresponder haplotypes. It is concluded that Ir genes can govern the ability to generate an IgM response upon initial exposure to antigen.
D000409:Alanine; D000818:Animals; D000917:Antibody Formation; D002478:Cells, Cultured; D002874:Chromosome Mapping; D004306:Dose-Response Relationship, Immunologic; D005796:Genes; D005799:Genes, Dominant; D008040:Genetic Linkage; D005971:Glutamates; D006639:Histidine; D006649:Histocompatibility Antigens; D007075:Immunoglobulin M / Q000096:biosynthesis*; D007519:Isoantigens; D008239:Lysine; D051379:Mice; D008815:Mice, Inbred Strains; D009578:Nitrobenzenes / Q000276:immunology*; D010455:Peptides / Q000276:immunology*; D013154:Spleen / Q000276:immunology; D014301:Trinitrobenzenes / Q000276:immunology*; D014443:Tyrosine
D005971:Glutamates; D006649:Histocompatibility Antigens; D007075:Immunoglobulin M; D007519:Isoantigens; D009578:Nitrobenzenes; D010455:Peptides; D014301:Trinitrobenzenes; D014443:Tyrosine; D006639:Histidine; D008239:Lysine; D000409:Alanine