The Journal of Experimental Medicine
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J. Exp. Med.
© The Rockefeller University Press
0022-1007/97/01/71/10 $2.00
Volume 185 January 1997 71-80

Scleroderma Autoantigens Are Uniquely Fragmented by Metal-catalyzed Oxidation Reactions: Implications for Pathogenesis

By Livia Casciola-Rosen,*Dagger Fredrick Wigley,§ and Antony Rosen§Dagger

From the * Department of Dermatology, § Department of Medicine, and Dagger  Department of Cell Biology & Anatomy, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

The observation that revelation of immunocryptic epitopes in self antigens may initiate the autoimmune response has prompted the search for processes which induce novel fragmentation of autoantigens as potential initiators of autoimmunity. The reversible ischemia reperfusion which characterizes scleroderma has focused attention on reactive oxygen species as molecules which might induce autoantigen fragmentation. We demonstrate that several of the autoantigens targeted in diffuse scleroderma are uniquely susceptible to cleavage by reactive oxygen species, in a metal-dependent manner. Multiple features of the fragmentation reaction and its inhibition indicate that these autoantigens possess metal-binding sites, which focus metal-catalyzed oxidation reactions (and consequent fragmentation) to specific regions of the antigens. These data suggest that the autoantibody response in scleroderma is the immune marker of unique protein fragmentation, induced by ischemia reperfusion in the presence of appropriate metals, and focus attention on abnormal metal status as a potential pathogenic principle in this disease.


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