Polyclonal activation autoimmunity

Furthermore, B cells and serum antibodies reactive with conventional antigens increased commensurately with those reactive with autoantigens. These results indicate that systemic autoimmune diseases arise from polyclonal B cell activation. These references are in PubMed. This may not be the complete list of references from this article. National Center for Biotechnology Information , U. Journal List J Exp Med v. J Exp Med. Copyright and License information Disclaimer.

Copyright notice. This article has been cited by other articles in PMC. Etiopathogenesis of murine SLE. Immunol Rev. The lupus autoantigens and the pathogenesis of systemic lupus erythematosus. Arthritis Rheum. Ly-1 B cells: functionally distinct lymphocytes that secrete IgM autoantibodies. J Immunol. The effect of polyclonal B-cell activation, brought about by injections of a B-cell activator-lipopolysaccharide from Gram-negative bacteria-is sufficient to cause autoimmune disease in an immunologically normal host.

In fact, autoimmune disease can be arrested if excessive polyclonal B-cell activation is suppressed; alternatively, autoimmune disease can be exacerbated if polyclonal B-cell activation is enhanced. We explore the mechanism of tissue injury when autoimmune disease is induced or exacerbated, and we consider the pathogenic roles of autoantibodies, immune complexes, complement, the blood cell carrier system, and the mononuclear phagocyte system.

Although polyclonal B-cell activation may be the mechanism whereby various factors can cause or exacerbate systemic autoimmune disease, polyclonal B-cell activation may cause autoimmune disease on its own. Abstract It is widely believed that autoimmunity is an integral part of the immune system, and that genetic, immunologic, hormonal, environmental and other factors contribute to the pathogenesis of autoimmune disease. Publication types Research Support, Non-U.