In vivo (Athens, Greece) · 2026
Negative Regulator of Interferon Response Promotes Toll-like Receptor 3-induced Interleukin 6 in Rheumatoid Synoviocyte.
СтатьяНазвание и аннотация: Перевод в очереди
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Wada Kairo, Imaizumi Tadaatsu, Ishibashi Hikaru Kristi, Nakamura Yuzuru, Saruga Tatsuro, Kawaguchi Shogo, Tachizaki Mayuki, Oishi Kazuki, Sasaki Eiji, Wada Kanichiro, Ishibashi Yasuyuki
Аннотация
BACKGROUND/AIM: Rheumatoid arthritis (RA) is an autoimmune disease, with synovial inflammation as an important symptom. However, the pathogenesis of RA has not been fully elucidated. Long noncoding RNAs play a role in various biological and pathological situations, and negative regulators of interferon response (NRIR) are long noncoding RNAs that regulate immune reactions. However, the role of NRIR in rheumatoid synovial inflammation remains unclear.
MATERIALS AND METHODS: Cultured human rheumatoid fibroblast-like synoviocytes (RFLS) were treated with a synthetic Toll-like receptor 3 (TLR3) ligand, polyinosinic:polycytidylic acid (poly I:C). Expression of NRIR was examined using reverse transcription-quantitative polymerase chain reaction. RNA interference against interferon-b (IFNB), nuclear factor-kappa B (NFKB) p65, and NRIR was performed by transfecting the cells with specific small interfering RNAs. Interleukin-6 (IL-6) protein levels in the culture medium were measured using an enzyme-linked immunosorbent assay kit. Phosphorylation of NF-kB p65 protein was determined using western blotting.
RESULTS: Treatment of cultured RFLS with poly I:C induced the expression of NRIR. Poly I:C-induced expression of NRIR was decreased by the knockdown of IFNB or NFKB p65. IL-6 induction by poly I:C was reduced by knockdown of NFKB p65 or NRIR, but not of IFNB. Knockdown of NRIR did not affect NF-kB p65 phosphorylation.
CONCLUSION: NRIR is induced by TLR3 signaling in RFLS. IFN-b and NF-kB are involved in NRIR induction via TLR3 signaling. NRIR is at least partially implicated in TLR3-mediated IL-6 expression in RFLS. NRIR may play a role in TLR3/IL-6-mediated inflammatory reactions in RFLS and may be a potential target for new therapeutic strategies against RA.
MATERIALS AND METHODS: Cultured human rheumatoid fibroblast-like synoviocytes (RFLS) were treated with a synthetic Toll-like receptor 3 (TLR3) ligand, polyinosinic:polycytidylic acid (poly I:C). Expression of NRIR was examined using reverse transcription-quantitative polymerase chain reaction. RNA interference against interferon-b (IFNB), nuclear factor-kappa B (NFKB) p65, and NRIR was performed by transfecting the cells with specific small interfering RNAs. Interleukin-6 (IL-6) protein levels in the culture medium were measured using an enzyme-linked immunosorbent assay kit. Phosphorylation of NF-kB p65 protein was determined using western blotting.
RESULTS: Treatment of cultured RFLS with poly I:C induced the expression of NRIR. Poly I:C-induced expression of NRIR was decreased by the knockdown of IFNB or NFKB p65. IL-6 induction by poly I:C was reduced by knockdown of NFKB p65 or NRIR, but not of IFNB. Knockdown of NRIR did not affect NF-kB p65 phosphorylation.
CONCLUSION: NRIR is induced by TLR3 signaling in RFLS. IFN-b and NF-kB are involved in NRIR induction via TLR3 signaling. NRIR is at least partially implicated in TLR3-mediated IL-6 expression in RFLS. NRIR may play a role in TLR3/IL-6-mediated inflammatory reactions in RFLS and may be a potential target for new therapeutic strategies against RA.