Desert dust induces TLR signaling to trigger Th2-dominant lung allergic inflammation via a MyD88-dependent signaling pathway
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ASD enhanced Th2 response in TLR2−/−, TLR4−/− and WT mice, but not in MyD88−/−.

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Th2 responses in TLR2−/− mice were attenuated by LPS inhibitor polymyxin B.

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TLR2 and TLR4 signaling is important in allergic lung disease aggravation by ASD.

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MyD88 is the key adapter molecule in the signaling pathway for Th2 activation.

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ASD-bound LPS and β-glucan may be strong candidates for the aggravating substances.

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