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The adaptor Act1 is required for interleukin 17-dependent signaling associated with autoimmune and inflammatory disease.

Nature immunology | Mar 16, 2007

T helper cells that produce interleukin 17 (IL-17) are associated with inflammation and the control of certain bacteria. We report here the essential involvement of the adaptor protein Act1 in IL-17 receptor (IL-17R) signaling and IL-17-dependent immune responses. After stimulation with IL-17, recruitment of Act1 to IL-17R required the IL-17R conserved cytoplasmic 'SEFIR' domain, followed by recruitment of the kinase TAK1 and E3 ubiquitin ligase TRAF6, which mediate 'downstream' activation of transcription factor NF-kappaB. IL-17-induced expression of inflammation-related genes was abolished in Act1-deficient primary astroglial and gut epithelial cells. This reduction was associated with much less inflammatory disease in vivo in both autoimmune encephalomyelitis and dextran sodium sulfate-induced colitis. Our data show that Act1 is essential in IL-17-dependent signaling in autoimmune and inflammatory disease.

Pubmed ID: 17277779 RIS Download

Mesh terms: Adaptor Proteins, Signal Transducing | Adoptive Transfer | Animals | Antigens, CD40 | Autoimmune Diseases | Autoimmunity | B-Cell Activation Factor Receptor | Colitis | Encephalomyelitis, Autoimmune, Experimental | Enzyme-Linked Immunosorbent Assay | Female | Fluorescent Antibody Technique | Gene Expression | Gene Expression Regulation | HeLa Cells | Humans | Inflammation | Interleukin-17 | Mice | Receptors, Interleukin-17 | Reverse Transcriptase Polymerase Chain Reaction | Signal Transduction | T-Lymphocytes | Transfection | Tumor Necrosis Factor Receptor-Associated Peptides and Proteins

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Associated grants

  • Agency: NIAID NIH HHS, Id: AI 065470

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