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Murine responses to immunization with 2, 4, 6-trinitrophenyl (TNP) conjugated to autogenous mouse serum albumin (MSA) in complete Freund's adjuvant (CFA) are controlled by a gene(s) in the K or I-A region of H-2 complex. High immune responses of both H-2d and H-2b mice have been mapped to this region of the major histocompatibility complex. No modifying effects were observed from genes to the right of I-A in either responder haplotype. High responsiveness controlled by Kb or I-Ab is inherited with complete or partial recessivity, depending on the route of immunization and the sex of the responder. However, high responsiveness controlled by Kd or I-Ad is inherited dominantly. This unusual pattern of inheritance of immune responsiveness to TNP-MSA is consistent with the genetic mapping to K or I-A. TNP-MSA-specific T-cell reactivity following immunization with TNP-MSA in vivo was examined utilizing a T-cell-dependent proliferation assay in vitro with cells obtained from high or low responder mice. Genetic mapping and mode of inheritance in this assay for antigen-specific T-cell reactivity corresponded with results obtained from a plaque-forming cell (PFC) assay measuring antibody production by B cells. Both the proliferative and PFC responses are probably under the same Ir gene control. Both gene dosage effects and Ir-gene-product interaction could influence the generation of specific immune responsiveness in F1 hybrids between high and low responders to TNP-MSA.

Original publication




Journal article



Publication Date





253 - 265


Animals, Mice, Inbred A, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Trinitrobenzenes, Serum Albumin, H-2 Antigens, Epitopes, Hemolytic Plaque Technique, Chromosome Mapping, Lymphocyte Activation, Antibody Formation, Major Histocompatibility Complex, Genes, Dominant, Phenotype, Haploidy, Female, Male