Systemic Lupus Erythematosus: From Genes to Organ Damage

Protocol
Part of the Methods in Molecular Biology book series (MIMB, volume 662)

Abstract

Systemic lupus erythematosus (SLE) is a disease characterized by inappropriate response to self-antigens. Genetic, environmental and hormonal factors are believed to contribute to the development of the disease. We think of SLE pathogenesis as occurring in three phases of variable duration. A series of regulatory failures during the ontogeny of the immune system lead to the emergence of auto-reactive clones and the production of auto-antibodies (phase I). As the immune response to self-antigens broadens, the auto-antibody repertoire is enriched (phase II) and clinical manifestations eventually ensue (phase III). The final result is tissue damage that if not treated will lead to the functional failure of such important organs as the kidney and brain.

Key words

Systemic Lupus Erythematosus Auto-antibodies Complement Cell signaling CD3ζ chain Fcγ receptor NFAT Nephritis 

Notes

Acknowledgments

This work was supported by the National Institute of Arthritis, Musculoskeletal and skin diseases grant No 1K23 AR055672-01A1

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© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  1. 1.Division of Rheumatology, Beth Israel Deaconess Medical CenterHarvard Medical SchoolBostonUSA

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