IL-17 induces production of IL-6 and IL-8 in rheumatoid arthritis synovial fibroblasts via NF-κB- and PI3-kinase/Akt-dependent pathways

التفاصيل البيبلوغرافية
العنوان: IL-17 induces production of IL-6 and IL-8 in rheumatoid arthritis synovial fibroblasts via NF-κB- and PI3-kinase/Akt-dependent pathways
المؤلفون: Hwang, Sue-Yun, Kim, Ju-Young, Kim, Kyoung-Woon, Park, Mi-Kyung, Moon, Youngmee, Kim, Wan-Uk, Kim, Ho-Youn
المصدر: Arthritis Research & Therapy
بيانات النشر: BioMed Central, 2004.
سنة النشر: 2004
مصطلحات موضوعية: rheumatoid arthritis, Interleukin-15, phosphatidylinositol 3-kinase, Receptors, Interleukin-17, Interleukin-6, Interleukin-17, Interleukin-8, Synovial Membrane, NF-kappa B, Transcription Factor RelA, Receptors, Interleukin, Fibroblasts, Middle Aged, Protein Serine-Threonine Kinases, Arthritis, Rheumatoid, IL-17, Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins, Humans, Mitogen-Activated Protein Kinases, fibroblast-like synoviocytes, Proto-Oncogene Proteins c-akt, Cells, Cultured, Research Article, Signal Transduction
الوصف: Recent studies of the pathogenesis of rheumatoid arthritis (RA) have revealed that both synovial fibroblasts and T cells participate in the perpetuation of joint inflammation as dynamic partners in a mutual activation feedback, via secretion of cytokines and chemokines that stimulate each other. In this study, we investigated the role of IL-17, a major Th1 cytokine produced by activated T cells, in the activation of RA synovial fibroblasts. Transcripts of IL-17R (IL-17 receptor) and IL-17RB (IL-17 receptor B) were present in fibroblast-like synoviocytes (FLS) of RA patients. IL-17R responded with increased expression upon in vitro stimulation with IL-17, while the level of IL-17RB did not change. IL-17 enhanced the production of IL-6 and IL-8 in FLS, as previously shown, but did not affect the synthesis of IL-15. IL-17 appears to be a stronger inducer of IL-6 and IL-8 than IL-15, and even exerted activation comparable to that of IL-1beta in RA FLS. IL-17-mediated induction of IL-6 and IL-8 was transduced via activation of phosphatidylinositol 3-kinase/Akt and NF-kappaB, while CD40 ligation and p38 MAPK (mitogen-activated protein kinase) are not likely to partake in the process. Together these results suggest that IL-17 is capable of more than accessory roles in the activation of RA FLS and provide grounds for targeting IL-17-associated pathways in therapeutic modulation of arthritis inflammation.
اللغة: English
تدمد: 1478-6362
1478-6354
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=pmid________::cbf27a06121514c8ebfc811c08e9ab59Test
http://europepmc.org/articles/PMC400429Test
حقوق: OPEN
رقم الانضمام: edsair.pmid..........cbf27a06121514c8ebfc811c08e9ab59
قاعدة البيانات: OpenAIRE