Perspectives
Nature Reviews Immunology 1, 147-153 (November 2001) | doi:10.1038/35100573
Opinion: From T to B and back again: positive feedback in systemic autoimmune disease
Mark J. Shlomchik1, Joseph E. Craft1 & Mark J. Mamula1 About the authors
Abstract
Systemic lupus erythematosus, a prototypical systemic autoimmune disease, is the result of a series of interactions within the immune system that ultimately lead to the loss of self-tolerance to nuclear autoantigens. Here, we present an integrated model that explains how self-tolerance is initially lost and how the loss of tolerance is then amplified and maintained as a chronic autoimmune state. Key to this model are the self-reinforcing interactions of T and B cells, which we suggest lead to perpetuation of autoimmunity as well as its spread to multiple autoantigen targets.
Author affiliations
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Mark J. Shlomchik is in the Department of Laboratory Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520-8035, USA.
Mark J. Shlomchik and Joseph E. Craft are in the Section of Immunobiology, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520-8035, USA.
Joseph E. Craft and Mark J. Mamula are in the Department of Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520-8035, USA.
Correspondence to: Mark J. Shlomchik1 Email: mark.shlomchik@yale.edu
