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. 2023 Feb 15;14:1093208. doi: 10.3389/fimmu.2023.1093208

Figure 2.

Figure 2

TLRs signalling in B cells and TLR7 and dysfunctional TLR9 compete for UNC93B1-dependent trafficking in SLE B cells. 1.When nucleic acid ligands are recognized by BCRs and internalized into B cells, they bind TLR7 or TLR9 in the late endosome; TLR7 or TLR9 then binds MyD88. MyD88 subsequently recruits the IRAK–TRAF6 complex, ultimately leading to activation of downstream NF-κB and AP1 signalling. 2.Dysfunctional TLR9 can lead to weakened competition of these TLRs for binding to UNC93B1 in endosomes, increasing TLR7 availability and resulting in higher TLR7 trafficking and responses, which manifest as autoimmune phenotypes.