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* Deutsches Rheumaforschungszentrum Berlin, Berlin, Germany;
Institut für Immunologie, Klinikum der Friedrich-Schiller-Universität Jena, Jena, Germany;
Institut für Medizinische Immunologie, Universitätsklinikum Charité, Berlin, Germany; and
Institut für Neuropathologie, Universität Göttingen, Göttingen, Germany
Infections sometimes associate with exacerbations of autoimmune diseases through pathways that are poorly understood. Ag-specific mechanisms such as cross-reactivity between a microbial Ag and a self-Ag have received no direct support. In this study, we show that injection of LPS induces experimental autoimmune encephalomyelitis in TCR-transgenic mice and relapse of encephalomyelitis in normal mice. This form of treatment induces proliferation and cytokine production in a fraction of effector/memory Th lymphocytes in vitro via physical contact of Th cells with CD4 LPS-responsive cells. TCR-mediated signals are not necessary; rather what is required is ligation of costimulatory receptors on Th cells by costimulatory molecules on the CD4 cells. This form of bystander activation provides an Ag-independent link between infection and autoimmunity that might fit the clinical and epidemiological data on the connection between infection and autoimmunity better than the Ag-specific models.
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