Abstract:
:Rheumatoid arthritis (RA) is an inflammatory disease with symmetric polyarthritis. IL-6 and NLRP3 inflammasome in macrophages contribute to the pathogenesis of RA. This study aimed to investigate the relationship between IL-6 and the NLRP3 inflammasome in RA. Here, we found that IL-6 inhibition reduced NLRP3 inflammasome activation in mice with collage-induced arthritis (CIA). In vitro studies showed that IL-6 directly induced NLRP3 inflammasome activation via cathepsin B (CTSB) in the presence of ATP. In addition, S100A9 induced by ATP stimulation promoted the interaction of CTSB and NLRP3 to activate the NLRP3 inflammasome. Our findings show a novel mechanism of NLRP3 inflammasome activation by IL-6 that may lead to a potential therapy for RA by interrupting the interaction between IL-6 and the NLRP3 inflammasome.
journal_name
Int Immunopharmacoljournal_title
International immunopharmacologyauthors
Wang H,Wang Z,Wang L,Sun L,Liu W,Li Q,Wang Jdoi
10.1016/j.intimp.2020.106985subject
Has Abstractpub_date
2020-11-01 00:00:00pages
106985eissn
1567-5769issn
1878-1705pii
S1567-5769(20)31204-2journal_volume
88pub_type
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doi:10.1016/j.intimp.2007.11.008
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