TY - JOUR
T1 - STAT4
T2 - genetics, mechanisms, and implications for autoimmunity.
AU - Korman, Benjamin D.
AU - Kastner, Daniel L.
AU - Gregersen, Peter K.
AU - Remmers, Elaine F.
N1 - Funding Information:
This work was supported by the National Institutes of Health (NIH) NO1-AR-2-2263 and RO1 AR44422 awards to Dr. Gregersen and by the Intramural Program of the National Institute of Arthritis, Musculoskeletal, and Skin Diseases. Dr. Korman was supported by the NIH Clinical Research Program, a public private partnership between the Foundation for the NIH and Pfizer.
PY - 2008/9
Y1 - 2008/9
N2 - 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.
AB - 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.
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U2 - 10.1007/s11882-008-0077-8
DO - 10.1007/s11882-008-0077-8
M3 - Review article
C2 - 18682104
AN - SCOPUS:55249101270
SN - 1529-7322
VL - 8
SP - 398
EP - 403
JO - Current Allergy and Asthma Reports
JF - Current Allergy and Asthma Reports
IS - 5
ER -