Journal
TRENDS IN IMMUNOLOGY
Volume 26, Issue 11, Pages 572-579Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2005.08.013
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Funding
- NIAMS NIH HHS [AR 47322, R01 AR047322-03, R01 AR050797-03, R01 AR047322, AR 50797, R01 AR050797] Funding Source: Medline
- NIDDK NIH HHS [DK 69282, R21 DK069282-02, R21 DK069282] Funding Source: Medline
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Systemic lupus erythematosus (SLE, lupus) results from immune-mediated damage to multiple organs. Its pathogenesis should be viewed as a series of steps, beginning with impaired immune regulation that permits self-reactive T-B-cell activation, which results in the production of autoantibodies. Activated T and B cells then infiltrate tissues, which along with autoantibody and immune complex deposition, triggering local events that ultimately cause organ damage. Although improved understanding of early autoimmune events might open up avenues for disease prevention, future investigations must focus on the mechanisms of end-organ damage in model systems and how to translate this knowledge into human disease. Understanding the mechanisms of each pathogenetic step would provide a rational basis for the development of disease stage-specific diagnostic markers and treatments.
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