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Joyce Rauch

Researcher at McGill University Health Centre

Publications -  111
Citations -  5666

Joyce Rauch is an academic researcher from McGill University Health Centre. The author has contributed to research in topics: Autoantibody & Lupus anticoagulant. The author has an hindex of 36, co-authored 108 publications receiving 5499 citations. Previous affiliations of Joyce Rauch include Scripps Research Institute & Brigham and Women's Hospital.

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Journal ArticleDOI

The antiphospholipid syndrome.

Jerrold S. Levine, +2 more
- 07 Mar 2002 - 
TL;DR: The broad spectrum of renal diseases that have been observed in association with this syndrome are discussed, and the impact that APS may have on pre-existing renal disease as well as current recommendations for treatment of APS are discussed.
Journal Article

Anti-phospholipid autoantibodies bind to apoptotic, but not viable, thymocytes in a beta 2-glycoprotein I-dependent manner.

Barbara E. Price, +8 more
- 01 Sep 1996 - 
TL;DR: It is proposed that the interaction of circulating beta 2GPI with redistributed anionic phospholipid may itself generate a novel ligand by which apoptotic cells are recognized directly for phagocytic clearance.
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Anti-dna antibody idiotypes in systemic lupus erythematosus

David A. Isenberg, +6 more
- 25 Aug 1984 - 
TL;DR: Levels of the 16/6/R idiotype tended to correlate with levels of antibodies to double-stranded DNA, but in some cases the clinical status was reflected better by the idiotype levels than by the levels of anti-double-Stranded-DNA antibodies.
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Antineutrophil Cytoplasmic Autoantibodies Interact with Primary Granule Constituents on the Surface of Apoptotic Neutrophils in the Absence of Neutrophil Priming

Hannah Gilligan, +9 more
- 01 Dec 1996 - 
TL;DR: It is shown by electron microscopy that apoptosis of unprimed PMN is also associated with the translocation of cytoplasmic granules to the cell surface and alignment just beneath an intact cell membrane, which provides a novel mechanism that is independent of priming.
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Apoptotic cells, at all stages of the death process, trigger characteristic signaling events that are divergent from and dominant over those triggered by necrotic cells: Implications for the delayed clearance model of autoimmunity.

Vimal A. Patel, +8 more
- 24 Feb 2006 - 
TL;DR: It is shown that apoptotic cells do not become proinflammatory upon the loss of membrane integrity and are inconsistent with the notion that delayed clearance alone can lead to autoimmunity.