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Autoimmunity and Lymphoproliferation: Two Genes are Worse than One

Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA

SUMMARY

Autoimmunity, first described as "horror autotoxicus" (fear of self-poisoning) by Paul Ehrlich in 1900, refers to the inability of one’s own immune system to recognize and discriminate its "self" from non-self or that which is foreign to the body. Defects in immune sureveillance leading to autoimmunity can result in occlusion of the vasculature, organ failure, and death. To better treat the specific disease states that arise from chronic autoimmunity, a greater understanding of the genetic factors that underlie much of autoimmunity (or the predisposition to it) must be garnered. A recent report demonstrates that mutations in both Fas (whose product directs the apoptosis of cells) and the Sle (systemic lupus erythematosus) locus in mice result in enhanced autoimmunity. Cohen provides a brief overview on autoimmunity with regard to SLE, and discusses what is known about the function of the genes in the Sle locus and how better therapies might arise from understanding how Sle and Fas proteins interact.

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