AKR/J gene(s) unlinked to H-2 determines dominant inheritance of lymphocyte hyporesponsiveness to acetylcholine receptor

T. J. Gorzynski, V. A. Lennon, R. M. Nathanson, C. S. David

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Abstract

Mice with the H-2(b) major histocompatibility complex haplotype are high immune responders to nicotinic acetylcholine receptors (AChR), whereas mice with the H-2(k) haplotype are generally low responders. F1 progeny of C57BL/6 (H-2(b)) mice crossed with mice of most H-2(k) strains are high responders to AChR in standard conditions of testing helper T cell proliferation in vitro (4 x 105 lymph node cells/microwell, 1 wk after primary challenge in vivo). In contrast, the F1 progeny of AKR/J (H-2(k)) crossed with high responder (H-2(b)) strains (B6, A.BY, or C3H.SW) were all hyporesponsive to AChR when lymphocytes were tested at 4 x 105 cells/well. However, at a density of 1 x 106 or greater/well, a high level of antigen-specific responsiveness was demonstrable in the F1 hybrid lymphocytes. A shift from low to high responsiveness to AChR at high cell densities was observed also in the H-2(b) strain AKR.B6. Other strains previously demonstrated to be low responders to AChR did not become responsive to AChR when lymphocyte numbers were increased to 1.4 x 106/well. The N2 generation yielded by backcrossing (AKR x B6)F1 mice to AKR/J were all low responders, whereas N2 progeny derived by backcrossing F1 to B6 were high or low responders in a ratio of approximately 1:1 (independent of their H-2 phenotype). Results consistent with this observation were obtained in (AKR x B6) F2 mice. These data suggest that at least one AKR/J gene outside of the H-2 complex exerts a hyporesponsive influence on the I-A-dependent helper T cell response to AChR in H-2(b) mice.

Original languageEnglish (US)
Pages (from-to)2079-2083
Number of pages5
JournalJournal of Immunology
Volume134
Issue number4
StatePublished - Jan 1 1985

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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