Experimental Models to Study Molecular Mechanisms Underlying Intestinal Inflammation
Charles O. Elson(University of Alabama at Birmingham), Yingzi Cong(University of Alabama at Birmingham), Steven L. Brandwein(University of Alabama at Birmingham), Casey T. Weaver(University of Alabama at Birmingham), Robert P. McCabe(University of Alabama at Birmingham), Michael Mähler(Jackson Laboratory), John P. Sundberg(Jackson Laboratory), Edward H. Leiter(Jackson Laboratory)
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Abstract
Experimental animal models, particularly the newer mouse models, have convincingly demonstrated that CD+ T cells play a central role in chronic intestinal inflammation. Such CD4+ effector T cells are induced by the bacterial flora. In at least one model, it is conventional protein antigens that are stimulating these pathogenic T cells. The antigens driving disease seem to be a selective subset of immunodominant proteins, likely derived from a subset of organisms. Multiple genes contribute to colitis susceptibility and a number of these genes are being localized.
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