Toll-like receptors (TLRs) are essential defensive mediators implicated in immune diseases. Tight regulation of TLR function is indispensable to avoid the damaging effects of chronic signaling. Several endogenous molecules have emerged as negative regulators of TLR signaling. In this review, we highlighted the structure, regulation, and function of RP105 and A20 in negatively modulating TLR-dependent inflammatory diseases, and in fibrosis and potential therapeutic approaches.
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Bale et al. (2021) studied this question.
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