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Systemic Lupus Erythematosus: From Genes to Organ Damage

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Systems Biology in Drug Discovery and Development

Part of the book series: Methods in Molecular Biology ((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.

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Acknowledgments

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

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Kyttaris, V.C. (2010). Systemic Lupus Erythematosus: From Genes to Organ Damage. In: Yan, Q. (eds) Systems Biology in Drug Discovery and Development. Methods in Molecular Biology, vol 662. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-800-3_13

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  • DOI: https://doi.org/10.1007/978-1-60761-800-3_13

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  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-60761-799-0

  • Online ISBN: 978-1-60761-800-3

  • eBook Packages: Springer Protocols

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