L
Livia Casciola-Rosen
Researcher at Johns Hopkins University School of Medicine
Publications - 168
Citations - 16003
Livia Casciola-Rosen is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Autoantibody & Dermatomyositis. The author has an hindex of 60, co-authored 153 publications receiving 14384 citations. Previous affiliations of Livia Casciola-Rosen include Johns Hopkins University.
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Journal ArticleDOI
Autoantigens targeted in systemic lupus erythematosus are clustered in two populations of surface structures on apoptotic keratinocytes.
TL;DR: Systemic lupus erythematosus is a multisystem autoimmune disease in which the autoantibody response targets a variety of autoantigens of diverse subcellular location, and it is shown that they are clustered in two distinct populations of blebs at the surface of apoptotic cells.
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Apopain/CPP32 cleaves proteins that are essential for cellular repair: a fundamental principle of apoptotic death.
Livia Casciola-Rosen,Donald W. Nicholson,Tae Chong,Kevin R. Rowan,Nancy A. Thornberry,Douglas K. Miller,Antony Rosen +6 more
TL;DR: The present studies demonstrate that U1-70kD and DNA-PKcs are excellent substrates for apopain, with cleavage occurring at sites that are highly similar to the cleavage site within PARP.
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Autoantibodies against 3‐hydroxy‐3‐methylglutaryl‐coenzyme A reductase in patients with statin‐associated autoimmune myopathy
Andrew L. Mammen,Tae Chung,Lisa Christopher-Stine,Paul Rosen,Antony Rosen,Kimberly R Doering,Livia Casciola-Rosen +6 more
TL;DR: Statins up-regulate the expression of HMGCR, the major target of autoantibodies in statin-associated IMNM, which may sustain the immune response even after statins are discontinued.
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Cleavage by granzyme B is strongly predictive of autoantigen status: implications for initiation of autoimmunity
TL;DR: It is shown that the majority of autoantigens targeted across the spectrum of human systemic autoimmune diseases are efficiently cleaved by granzyme B in vitro and during cytotoxic lymphocyte granule–induced death, generating unique fragments not observed during any other form of apoptosis.
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Surface blebs on apoptotic cells are sites of enhanced procoagulant activity: implications for coagulation events and antigenic spread in systemic lupus erythematosus.
TL;DR: It is proposed that the PtdSer exposed on the outside of these blebs can induce the production of anti-phospholipid antibodies, which might also enhance the immunogenicity of the bleb contents.