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
|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||Animals — Antigens, Thy-1/immunology — Autoantibodies/ biosynthesis — B-Lymphocytes/ immunology/metabolism — Base Sequence — Bone Marrow/immunology — Female — Isoantibodies/pharmacology — Lupus Erythematosus, Systemic/ etiology/ genetics — Lymphocyte Cooperation/ genetics — Lymphocyte Depletion — Male — Mice — Mice, Inbred C57BL — Mice, Mutant Strains — Molecular Sequence Data — Radiation Chimera — Syndrome — T-Lymphocytes/ immunology — Y Chromosome/ genetics/ immunology|
This document has no fulltext available yet, but you can contact its author by using the form below.
|FOSSATI-JIMACK, Liliane et al. 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. In: European Journal of Immunology, 1995, vol. 25, n° 12, p. 3412-3417. doi: 10.1002/eji.1830251231 https://archive-ouverte.unige.ch/unige:10897|