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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
Author(s) -
Fossati Liliane,
Sobel Eric S.,
Iwamoto Masahiro,
Cohen Philip L.,
Eisenberg Robert A.,
Izui Shozo
Publication year - 1995
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830251231
Subject(s) - biology , autoantibody , systemic lupus erythematosus , immunology , germinal center , bone marrow , autoimmune disease , autoimmunity , antigen , microchimerism , b cell , antibody , microbiology and biotechnology , genetics , disease , medicine , fetus , pregnancy
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.

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