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Lack of TAK1 in dendritic cells inhibits the contact hypersensitivity response induced by trichloroethylene in local lymph node assay
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文摘

Lack of TAK1 in DC caused an abolished TCE-induced CHS response.

TAK1 in DCs was essential to maintain the homeostasis of T cells in TCE-induced CHS.

Intact TAK1 in DCs was critical to promote T-cell priming in TCE-induced CHS.

DC-specific TAK1 deficiency abolished the TCE-mediated phosphorylation of Jnk.

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