Impaired contact hypersensitivity to trinitrochlorobenzene in interleukin‐4‐deficient mice

We have examined the role of endogenously produced interleukin‐4 (IL‐4) in the contact hypersensitivity (CH) reaction to the haptene trinitrochlorobenzene (TNCB). The CH reaction was abolished in IL‐4 genetically deficient mice (IL‐4 KO), when compared to wild‐type (wt) mice. The CH reaction was res...

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