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. Author manuscript; available in PMC: 2012 Jul 22.
Published in final edited form as: Immunity. 2011 Jul 22;35(1):3–5. doi: 10.1016/j.immuni.2011.07.006

Figure 1. Unc93B1 control of TLR7 and TLR9 trafficking into signaling endosomes.

Figure 1

B cells, plasmacytoid DCs, DCs and macrophages express TLR7 and TLR9. At steady state, the majority of TLR7 and TLR9 reside in the ER in cells expressing WT Unc93B1. Upon TLR stimulation, TLR9 is preferentially transported through the early endosome to the acidified endosomes by Unc93B1, whereby it is cleaved to become competent for signaling. In contrast, D34A mutant Unc93B1 transports TLR7, but not TLR9, to the signaling endosome even in the absence of external stimuli. Stimulation of TLR7 by endogenous RNA ligands results in B cell-dependent Th1 and Th17 cell differentiation, which leads to splenomegaly with myeloproliferation, thrombocytopenia, hepatic necrosis and death.