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Osteoarthritis and Toll-Like Receptors: When Innate Immunity Meets Chondrocyte Apoptosis

1
Department of Rheumatology, Helsinki University and Helsinki University Hospital, 00014 Helsinki, Finland
2
Translational Immunology Research Program, University of Helsinki, 00014 Helsinki, Finland
3
Orton Research Institute, 00280 Helsinki, Finland
*
Author to whom correspondence should be addressed.
Biology 2020, 9(4), 65; https://doi.org/10.3390/biology9040065
Received: 24 February 2020 / Revised: 26 March 2020 / Accepted: 28 March 2020 / Published: 30 March 2020
Osteoarthritis (OA) has long been viewed as a degenerative disease of cartilage, but accumulating evidence indicates that inflammation has a critical role in its pathogenesis. In particular, chondrocyte-mediated inflammatory responses triggered by the activation of innate immune receptors by alarmins (also known as danger signals) are thought to be involved. Thus, toll-like receptors (TLRs) and their signaling pathways are of particular interest. Recent reports suggest that among the TLR-induced innate immune responses, apoptosis is one of the critical events. Apoptosis is of particular importance, given that chondrocyte death is a dominant feature in OA. This review focuses on the role of TLR signaling in chondrocytes and the role of TLR activation in chondrocyte apoptosis. The functional relevance of TLR and TLR-triggered apoptosis in OA are discussed as well as their relevance as candidates for novel disease-modifying OA drugs (DMOADs). View Full-Text
Keywords: osteoarthritis; chondrocytes; toll-like receptors; apoptosis; innate immunity; cartilage osteoarthritis; chondrocytes; toll-like receptors; apoptosis; innate immunity; cartilage
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Barreto, G.; Manninen, M.; K. Eklund, K. Osteoarthritis and Toll-Like Receptors: When Innate Immunity Meets Chondrocyte Apoptosis. Biology 2020, 9, 65.

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