Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6118975 | Joint Bone Spine | 2014 | 5 Pages |
Abstract
Deficiency of TLRs or their signalling molecule MyD88 did not impact on the severity of experimental OA. Our results demonstrate that MyD88-dependent TLRs are not involved in this murine OA model. Moreover, the dispensable role of MyD88, which is also an adaptor for IL-1 receptor signaling, suggests that IL-1 is not a key mediator in the development of OA. This latter hypothesis is strengthened by the lack of efficiency of IL-1β antagonist in the treatment of OA.
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Authors
Sonia Nasi, Hang-Korng Ea, Véronique Chobaz, Peter van Lent, Frédéric Lioté, Alexander So, Nathalie Busso,