STAT4: genetics, mechanisms, and implications for autoimmunity.

Benjamin D. Korman*, Daniel L. Kastner, Peter K. Gregersen, Elaine F. Remmers

*Corresponding author for this work

Research output: Contribution to journalReview article

113 Scopus citations

Abstract

Recent advances in genetics and technology have led to breakthroughs in understanding the genes that predispose individuals to autoimmune diseases. A common haplotype of the signal transducer and activator of transcription 4 (STAT4) gene has been shown to be associated with susceptibility to rheumatoid arthritis, systemic lupus erythematosus, and primary Sjögren's syndrome. STAT4 is a transcription factor that transduces interleukin-12, interleukin-23, and type 1 interferon cytokine signals in T cells and monocytes, leading to T-helper type 1 and T-helper type 17 differentiation, monocyte activation, and interferon-gamma production. Although the evidence for this association is very strong and well replicated, the exact mechanism by which polymorphisms in this gene lead to disease remains unknown. In concert with the identification of other disease-associated loci, elucidating how the variant form of STAT4 modulates immune function should lead to an improved understanding of the pathophysiology of autoimmunity.

Original languageEnglish (US)
Pages (from-to)398-403
Number of pages6
JournalCurrent allergy and asthma reports
Volume8
Issue number5
DOIs
StatePublished - Sep 2008

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pulmonary and Respiratory Medicine

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    Korman, B. D., Kastner, D. L., Gregersen, P. K., & Remmers, E. F. (2008). STAT4: genetics, mechanisms, and implications for autoimmunity. Current allergy and asthma reports, 8(5), 398-403. https://doi.org/10.1007/s11882-008-0077-8