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Erschienen in: Inflammation 3/2023

10.03.2023 | REVIEW

Therapeutic Potential of Targeting the NLRP3 Inflammasome in Rheumatoid Arthritis

verfasst von: Jie Gao, Hongliang Zhang, Yanyan Yang, Jinhui Tao

Erschienen in: Inflammation | Ausgabe 3/2023

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Abstract

NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a cytoplasmic multiprotein complex composed of the innate immune receptor protein NLRP3, the adapter protein apoptosis-associate speck-like protein containing a caspase recruitment domain (ASC), and the inflammatory protease cysteine-1. Pathogen-associated molecular patterns (PAMPs) or other endogenous danger-associated molecular patterns (DAMPs) activate the NLRP3 inflammasome. As part of the innate immune response, activated NLRP3 promotes GSDMD-dependent pyroptosis, and IL-1β and IL-18 are released during inflammation. Aberrantly activated NLRP3 is deeply involved in various inflammatory diseases. Due to its interaction with adaptive immunity. NLRP3 inflammation has increasingly received attention in autoimmune diseases. Rheumatoid arthritis (RA) is a classic autoimmune disease, which mainly causes bone and cartilage damage. Elevated levels of NLRP3 can be detected in the synovium of RA patients. NLRP3 overactivation is strongly associated with RA activity. Mouse models of spontaneous arthritis has shown that NLRP3/IL-1β axis is implicated in periarticular inflammation in RA. In this review, we describe the current understanding of NLRP3 activation in RA pathogenesis and dissect its impact on innate and adaptive immunity. We also discuss the potential application of specific inhibitors of NLRP3 to provide new therapeutic strategies for treating RA.
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Metadaten
Titel
Therapeutic Potential of Targeting the NLRP3 Inflammasome in Rheumatoid Arthritis
verfasst von
Jie Gao
Hongliang Zhang
Yanyan Yang
Jinhui Tao
Publikationsdatum
10.03.2023
Verlag
Springer US
Erschienen in
Inflammation / Ausgabe 3/2023
Print ISSN: 0360-3997
Elektronische ISSN: 1573-2576
DOI
https://doi.org/10.1007/s10753-023-01795-5

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