Rheumatology 1999; 38: 1177-1183
© 1999 British Society for Rheumatology
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The role of apoptosis in systemic lupus erythematosus
Division of Immunity and Infection, The University of Birmingham, Birmingham B15 2TT, UK
Correspondence to:
M. Salmon, Division of Immunity and Infection, Rheumatology Research Group, The Medical School, The University of Birmingham, Birmingham B15 2TT, UK.
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Introduction |
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When it was described by Kerr et al. [1], the phenomenon of apoptosis, or programmed cell death, was greeted with a resounding lack of interest. The importance of this phenomenon is such that it is now very difficult to pick up any journal in a biomedical field without finding at least one paper on the subject. It has become apparent that the process is ubiquitous, representing a vital part of growth and differentiation in all tissues. The fundamental mechanisms of apoptosis and the genes that control it are highly conserved between species as diverse as worms and humans [2, 3].
Immunological research in apoptosis has focused on three areas in particular: (1) the selection of new lymphocytes, both B and T cells, before antigen challenge [4–6]; (2) the regulation of clonal expansion and resolution, including the elimination of apoptotic cells
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Apoptosis |
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A question of tolerance |
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Systemic lupus erythematosus as a disease of defective apoptosis |
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Too much apoptosis? |
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Somatic hypermutation and B-cell memory |
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A conundrum |
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Why is the clearance of apoptotic cells deficient in patients with SLE? |
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A vicious circle of C1q |
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Acknowledgments |
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References |
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