Rheumatology Advance Access originally published online on February 8, 2006
Rheumatology 2006 45(5):500-501; doi:10.1093/rheumatology/kel036
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
EDITORIAL |
The effect of UVB on lupus skin: new light on the role of apoptosis in the pathogenesis of autoimmunity
Center of Experimental Rheumatology and Department of Rheumatology, University Hospital, Zurich, Switzerland and 1 Medical Research Service, Durham Veterans Administration Hospital and Departments of Medicine and Immunology, Duke University Medical Center, Durham, NC, USA
Correspondence to: O. Distler. E-mail: oliver.distler@usz.ch
| The first 150 words of the full text of this article appear below. |
Apoptosis is a major form of programmed cell death and occurs in both physiological and pathological conditions. With apoptosis, cells display distinct morphological and biochemical features that allow their identification and enumeration both in vivo and in vitro. Prominent changes in cells undergoing this process are chromatin condensation, DNA fragmentation, membrane blebbing and externalization of phosphatidylserine of the cell membrane [1]. Once apoptosis is initiated, alterations in membrane structure mark a cell for recognition by macrophages that can engulf the dying cell for safe disposal. Indeed, the phagocytosis of dead cells is one of the critical functions of the immune system in preventing inadvertent immune activation by proinflammatory cellular material arising during death. Given the potential impact of dying cells and their products on the immune system, disturbances of the cell death and clearance processes have been postulated to occur in a variety of human diseases, including