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The Journal of Immunology, 2005, 175: 104-111.
Copyright © 2005 by The American Association of Immunologists

The Influence of Effector T Cells and Fas Ligand on Lupus-Associated B Cells 1

Michele L. Fields, Simone A. Nish, Brian D. Hondowicz, Michele H. Metzgar, Gina N. Wharton, Andrew J. Caton and Jan Erikson2

The Wistar Institute, Room 276, 3601 Spruce Street, Philadelphia, PA 19104

Circulating autoantibodies against dsDNA and chromatin are a characteristic of systemic lupus erythematosus in humans and many mouse models of this disease. B cells expressing these autoantibodies are normally regulated in nonautoimmune-prone mice but are induced to secrete Abs following T cell help. Likewise, anti-chromatin autoantibody production is T cell-dependent in Fas/Fas ligand (FasL)-deficient (lpr/lpr or gld/gld) mice. In this study, we demonstrate that Th2 cells promote anti-chromatin B cell survival and autoantibody production in vivo. FasL influences the ability of Th2 cells to help B cells, as Th2-gld/gld cells support higher titers of anti-chromatin Abs than their FasL-sufficient counterparts and promote anti-chromatin B cell participation in germinal centers. Th1 cells induce anti-chromatin B cell germinal centers regardless of FasL status; however, their ability to stimulate anti-chromatin Ab production positively correlates with their level of IFN-{gamma} production. This distinction is lost if FasL-deficient T cells are used: Th1-gld/gld cells promote significant titers of anti-chromatin Abs regardless of IFN-{gamma} production levels. Thus, FasL from effector T cells plays an important role in determining the fate of anti-chromatin B cells.


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