Experimental atopic dermatitis depends on IL-33R signaling via MyD88 in dendritic cells

@inproceedings{Li2017ExperimentalAD,
  title={Experimental atopic dermatitis depends on IL-33R signaling via MyD88 in dendritic cells},
  author={Changwei Li and Isabelle Maillet and Claire Mackowiak and Camille Viala and Franco Di Padova and Mei Li and Dieudonn{\'e}e Togb{\'e} and Val{\'e}rie F. J. Quesniaux and Yuping Lai and Bernhard Ryffel},
  booktitle={Cell death & disease},
  year={2017}
}
Atopic dermatitis (AD) is a chronic Th2 type inflammatory skin disorder. Here we report that MyD88 signaling is crucial in the pathogenesis of experimental AD induced by vitamin D3 analog MC903. The clinical signs and inflammation caused by MC903 are drastically reduced in MyD88-/- mice with diminished eosinophil, neutrophil infiltration and Th2 cytokine expression. The biological effect of interleukin-1 (IL-1) family members relies on MyD88 signaling. We observed a strong upregulation of IL-1… CONTINUE READING
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