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Ultraviolet light-induced keratinocyte apoptosis: A potential mechanism for the induction of skin lesions and autoantibody production in LE
L. Casciola-Rosen
Department of Dermatology, John Hopkins University School of Medicine, Department of Cell Biology & Anatomy, John Hopkins University School of Medicine, 720 Rutland Avenue, Room 1055, Baltimore, MD 21205, USA
A. Rosen
Department of Medicine, John Hopkins Univesity School of Medicine, Department of Cell Biology & Anatomy, John Hopkins University School of Medicine, 720 Rutland Avenue, Room 1055, Baltimore, MD 21205, USA
Systemic lupus erythematosus (SLE) is a prototype systemic autoimmune disease which is characterized clinically by pleiotropy and periodicity. The immune features which accompany the characteristic flares of the disease have strongly suggested that the autoimmune response is driven by self antigen, and is T cell-dependent. These features have prompted the search for potential initiating process(es) which induce the release of self-antigens in a form which causes T cell tolerance to those self molecules to be broken. We review here several recent observations which implicate apoptotic cells as an important potential source of clustered and concentrated autoantigens in SLE, and present our current model whereby the novel autoantigen fragments generated in apoptotic surface blebs initiate and drive the autoimmune response in this disease.
Key Words: Lupus • keratinocytes • apoptosis • autoantibody • ICE
Lupus, Vol. 6, No. 2,
175-180 (1997)
DOI: 10.1177/096120339700600213
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