NDLI: Synoviocyte innate immune responses: I. Differential regulation of interferon responses and the JNK pathway by MAPK kinases.

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Synoviocyte innate immune responses: I. Differential regulation of interferon responses and the JNK pathway by MAPK kinases.

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Synoviocyte innate immune responses: I. Differential regulation of interferon responses and the JNK pathway by MAPK kinases.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Sweeney, Susan E. Firestein, Gary S. Yoshizawa, Toshio Hammaker, Deepa Boyle, David L.
Description	Country affiliation: United States Author Affiliation: Yoshizawa T ( Division of Rheumatology, Allergy and Immunology, University of California, San Diego School of Medicine, La Jolla, CA 92093, USA.)
Abstract	JNK is a key regulator of matrix metalloproteinase production in rheumatoid arthritis. It is regulated by two upstream kinases known as MKK4 and MKK7. Previous studies demonstrated that only MKK7 is required for cytokine-mediated JNK activation and matrix metalloproteinase expression in cultured fibroblast-like synoviocytes (FLS). However, the functions of MKK4 and MKK7 in synoviocyte innate immune responses have not been determined. TNF, peptidoglycan (PGN), and LPS stimulation led to higher and more prolonged MKK7 phosphorylation compared with MKK4 in FLS. However, this pattern was reversed in poly(I-C) stimulated cells. siRNA knockdown studies showed that TNF, PGN, and LPS-induced JNK and c-Jun phosphorylation are MKK7 dependent, while poly(I-C) responses require both MKK4 and MKK7. Poly(I-C)-induced expression of IP-10, RANTES, and IFN-beta mRNA was decreased in MKK4- or MKK7-deficient FLS. However, MKK4 and MKK7 deficiency did not affect phosphorylation of IkappaB kinase-related kinases in the TLR3 signaling pathway. MKK7, but not MKK4 deficiency, significantly decreased poly(I-C)-mediated IRF3 dimerization, DNA binding, and IFN-sensitive response element-mediated gene transcription. These results were mimicked by the JNK inhibitor SP600125, indicating that JNK can directly phosphorylate IRF3. In contrast, deficiency of either MKK4 or MKK7 decreased AP-1 transcriptional activity. Therefore, JNK is differentially regulated by MKK4 and MKK7 depending on the stimulus. MKK7 is the primary activator of JNK in TNF, LPS, and PGN responses. However, TLR3 requires both MKK4 and MKK7, with the former activating c-Jun and the latter activating both c-Jun and IRF3 through JNK-dependent mechanisms.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	5
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Immunity, Innate Interferons Jnk Mitogen-activated Protein Kinases Metabolism Mitogen-activated Protein Kinase Kinases Physiology Synovial Fluid Immunology Arthritis, Rheumatoid Pathology Interferon Regulatory Factor-3 Interferon-beta Genetics Map Kinase Kinase 4 Map Kinase Kinase 7 Phosphorylation Cytology Toll-like Receptor 3 Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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