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Abnormalities of T cell signaling in systemic lupus erythematosus

Journal

ARTHRITIS RESEARCH & THERAPY
Volume 13, Issue 2, Pages -

Publisher

BIOMED CENTRAL LTD
DOI: 10.1186/ar3251

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Funding

  1. Rigel pharmaceuticals, San Francisco, CA
  2. NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI042269] Funding Source: NIH RePORTER

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Systemic lupus erythematosus (SLE) is an autoimmune disease resulting from a loss of tolerance to multiple self antigens, and characterized by autoantibody production and inflammatory cell infiltration in target organs, such as the kidneys and brain. T cells are critical players in SLE pathophysiology as they regulate B cell responses and also infiltrate target tissues, leading to tissue damage. Abnormal signaling events link to defective gene transcription and altered cytokine production, contributing to the aberrant phenotype of T cells in SLE. Study of signaling and gene transcription abnormalities in SLE T cells has led to the identification of novel targets for therapy.

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