Journal
AUTOIMMUNITY REVIEWS
Volume 15, Issue 1, Pages 1-8Publisher
ELSEVIER
DOI: 10.1016/j.autrev.2015.08.009
Keywords
Toll-like receptors; Rheumatoid arthritis; Innate immunity; Osteoclasts
Categories
Funding
- NIAMS/NIH [AR62173]
- Shriners Hospitals for Children [SHC 250862]
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR062173] Funding Source: NIH RePORTER
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Toll-like receptors (TLRs) constitute an important mechanism in the activation of innate immune cells including monocytes, macrophages and dendritic cells. Macrophage activation by TLRs is pivotal in the initiation of the rapid expression of pro-inflammatory cytokines TNF, IL-1 beta and IL-6 while promoting Th17 responses, all of which play critical roles in autoimmunity. Surprisingly, in inflammatory arthritis, activation of specific TLRs can not only induce but also inhibit cellular processes associated with bone destruction. The intercellular and intracellular orchestration of signals from different TLRs, their endogenous or microbial ligands and accessory molecules determine the activating or inhibitory responses. Herein, we review the TLR-mediated activation of innate immune cells in their activation and differentiation to osteoclasts and the capacity of these signals to contribute to bone destruction in arthritis. Detailed understanding of the opposing mechanisms of TLRs in the induction and suppression of cellular processes in arthritis may pave the way to develop novel therapies to treat autoimmunity. (C) 2015 Elsevier B.V. All rights reserved.
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