NDLI: CIKS/Act1-mediated signaling by IL-17 cytokines in context: implications for how a CIKS gene variant may predispose to psoriasis.

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CIKS/Act1-mediated signaling by IL-17 cytokines in context: implications for how a CIKS gene variant may predispose to psoriasis.

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CIKS/Act1-mediated signaling by IL-17 cytokines in context: implications for how a CIKS gene variant may predispose to psoriasis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Johnson, Peter F. Paun, Andrea Sønder, Søren Ulrik Ha, Hye-Lin Siebenlist, Ulrich
Description	Country affiliation: United States Author Affiliation: Sønder SU ( Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.)
Abstract	Psoriasis is a relapsing skin disease characterized by abnormal keratinocyte proliferation and differentiation and by an influx of inflammatory immune cells. Recently, IL-17 cytokines have been strongly implicated as critical for the pathogenesis of this disease. IL-17A (also known as IL-17) and IL-17F are the signature cytokines of Th17 cells, but are also produced by innate cells, including Î³Î´ T cells present in skin, whereas epithelial cells, including keratinocytes, may produce IL-17C. IL-17 cytokines signal via the adaptor protein connection to IκB kinase and stress-activated protein kinases (CIKS)/Act1. Psoriasis is a disease with a strong genetic predisposition, and the gene encoding CIKS has recently been identified as a susceptibility locus. Unexpectedly, one predisposing gene variant features a mutation that impairs rather than enhances CIKS-mediated IL-17 cytokine signaling, counter to the predicted role for IL-17 cytokines in psoriatic inflammation. In this study, we demonstrate, however, that this mutant adaptor does not impair the IL-17-specific contributions to the genetic response when combined with TNF- , a cytokine also prominent in psoriatic inflammation. Interestingly, TNF- signals compensate IL-17 signaling defects imposed by this mutant adaptor even for genes that are not induced by TNF- alone, including the transcription factors CCAAT/enhancer binding protein Î´ and IκBÎ¶, which help regulate secondary gene expression in response to IL-17. Based on these findings we discuss a scenario in which the mutant adaptor may interfere with homeostatic maintenance of epithelial barriers, thereby potentially enabling the initiation of inflammatory responses to insults, whereas this same mutant adaptor would still be able to mediate IL-17-specific contributions to inflammation once TNF- is present.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1103233
Journal	The Journal of Immunology
Issue Number	12
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Genetic Predisposition To Disease Genetics Interleukin-17 Immunology Psoriasis Signal Transduction Tumor Necrosis Factor Receptor-associated Peptides And Proteins Animals Blotting, Western Cytokines Metabolism Flow Cytometry Mice Mice, Knockout Polymorphism, Single Nucleotide Real-time Polymerase Chain Reaction Research Support, N.i.h., Intramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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