Two distinct high immune response phenotypes are both controlled byH-2 genes mapping inK orI-A

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Abstract
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 theK orI-A region of theH-2 complex. High immune responses of bothH-2 d andH-2 b mice have been mapped to this region of the major histocompatibility complex. No modifying effects were observed from genes to the right ofI-A in either responder haplotype. High responsiveness controlled byK b orI-A b is inherited with complete or partial recessivity, depending on the route of immunization and the sex of the responder. However, high responsiveness controlled byK d orI-A d is inherited dominantly. This unusual pattern of inheritance of immune responsiveness to TNP-MSA is consistent with the genetic mapping toK orI-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 sameIr 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.