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.