A shedding soluble form of interleukin-17 receptor D exacerbates collagen-induced arthritis through facilitating TNF-α-dependent receptor clustering.
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ABSTRACT:
SUBMITTER: Liu S
PROVIDER: S-EPMC8322419 | biostudies-literature | 2021 Aug
REPOSITORIES: biostudies-literature
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A shedding soluble form of interleukin-17 receptor D exacerbates collagen-induced arthritis through facilitating TNF-α-dependent receptor clustering.
Liu Sihan S Fu Yanxia Y Mei Kunrong K Jiang Yinan Y Sun Xiaojun X Wang Yinyin Y Ren Fangli F Jiang Congshan C Meng Liesu L Lu Shemin S Qin Zhihai Z Dong Chen C Wang Xinquan X Chang Zhijie Z Yang Shigao S
Cellular & molecular immunology 20200922 8
Rheumatoid arthritis (RA) is exacerbated by TNF-alpha signaling. However, it remains unclear whether TNF-α-activated TNFR1 and TNFR2 are regulated by extracellular factors. Here, we showed that soluble glycosylated interleukin-17 receptor D (sIL-17RD), which was produced by proteolytic cleavage, enhanced TNF-α-induced RA. We revealed that IL-17RD shedding was induced by the proteolytic enzyme TACE and enhanced by TNF-α expression in macrophages. Intriguingly, sIL-17RD was elevated in the sera of ...[more]
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