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The Yaa gene-mediated acceleration of murine lupus: Yaa- T cells from non-autoimmune mice collaborate with Yaa+ B cells to produce lupus autoantibodies in vivo

Fossati-Jimack, Liliane
Sobel, E. S.
Iwamoto, Masahiro
Cohen, P. L.
Eisenberg, R. A.
Published in European Journal of Immunology. 1995, vol. 25, no. 12, p. 3412-3417
Abstract The BXSB Y chromosome-linked mutant gene, Yaa, promotes autoimmune responses in mice predisposed to a lupus-like autoimmune disease. We have previously shown that a cognate interaction of T cells with B cells expressing the Yaa gene appears to be responsible for the accelerated production of autoantibodies. To investigate whether T cells that provide help for autoantibody production by Yaa+ B cells need to express the Yaa gene, we have made radiation bone marrow chimeras containing two sets of T and B cells from mice with or without the Yaa gene and differing by the Thy-1 and Igh allotypes. We then determined autoantibody production following the selective elimination of T cells of Yaa+ origin by treating mice with allele-specific anti-Thy-1 monoclonal antibody. Our results demonstrated that the selective production of autoantibodies by Yaa+ B cells in Yaa(+)-Yaa- double bone marrow chimeras can be mediated as efficiently by T cells from non-autoimmune mice lacking the Yaa gene as by T cells from autoimmune mice bearing the Yaa gene. This indicates that T cells from non-autoimmune Yaa- mice are capable of providing help for autoimmune responses by collaborating with Yaa+ B cells. These data thus strongly suggest that the Yaa gene defect is not functionally expressed in T cells, but only in B cells, and contrast with parallel experiments in the lpr model, in which defects of the Fas antigen in both T and B cells are crucial for the lpr gene-mediated promotion of autoantibody production.
Keywords AnimalsAntigens, Thy-1/immunologyAutoantibodies/ biosynthesisB-Lymphocytes/ immunology/metabolismBase SequenceBone Marrow/immunologyFemaleIsoantibodies/pharmacologyLupus Erythematosus, Systemic/ etiology/ geneticsLymphocyte Cooperation/ geneticsLymphocyte DepletionMaleMiceMice, Inbred C57BLMice, Mutant StrainsMolecular Sequence DataRadiation ChimeraSyndromeT-Lymphocytes/ immunologyY Chromosome/ genetics/ immunology
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PMID: 8566031
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