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In normal mouse strains, the T cell proliferative response to the nuclear autoantigen Sm is under MHC-linked Ir gene control. Autoimmune MRL/Mp-+/+ (+/+) mice, which spontaneously make anti-Sm antibodies, have the nonresponder H-2k MHC genotype, yet their T cells respond to mouse Sm. In the present study, we have used Sm-reactive continuous T cell lines to show that the Sm responsiveness of +/+ T cells is not due to aberrancy of the Iak molecules expressed on +/+ antigen-presenting cells. Additionally, the failure of normal Iak mouse strains to respond to mouse Sm could not be attributed to the influence of suppressor cells. Therefore, the response of +/+ mice to mouse Sm is probably due to the development of an abnormal repertoire of T cells capable of recognizing self-antigens in the context of Ia. Analyses of F1 hybrid and backcross mice indicated that their responsiveness was inherited in a dominant manner, probably as a single gene not linked to H-2. Further investigation of this gene and its mode of action may lead to increased understanding of the mechanisms of spontaneous autoimmunity in SLE mice.
Bernard et al. (1985) studied this question.