How are Th2 antigens recognized by DCs?
So far we have very little knowledge of which pathogen-derived molecules bind to which receptors on DCs to confer Th2-inductive capacity. TLRs and MyD88 have been implicated in this process: ligation of TLR2 can induce a Th2 response via extracellular signal-regulated kinase phosphorylation and stabilization of the transcription factor c-Fos (24, 27), schistosome sugars can act via TLR4 to condition Th2-driving DCs (28), and schistosome lipids bind TLR2 to induce IL-10–producing Tr1 cells (23). The triggering of TLR2/MyD88 by EDN shown by Yang et al. (6) is therefore consistent with these other reports of Th2-associated DC stimuli. But conclusive evidence that TLRs or MyD88 have a fundamental role in directing DCs to induce Th2 responses is lacking. And because DC-driven Th2 induction can occur in an MyD88-independent fashion (14), it may be that Th2 responsiveness is not as dependent on the MyD88 pathway as is Th1. Recently, C-type lectin receptors (CLRs) have drawn attention both as
