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.
Citation: Swarna Bale, John Varga, Swati Bhattacharyya. Role of RP105 and A20 in negative regulation of toll-like receptor activity in fibrosis: potential targets for therapeutic intervention[J]. AIMS Allergy and Immunology, 2021, 5(2): 102-126. doi: 10.3934/Allergy.2021009
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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