Lly understood. Objectives: We sought to determine the mechanisms how TGF- signaling through Smad4 regulates the pathogenic effector T cell subsets in CHS. Methods: We used Cd4Cre-loxp system to delete Smad4 in T cellspecific manner (Cd4Cre;Smad4fl/fl,+/+). Cd4Cre;Smad4fl/fl,+/+ mice were immunized and sensitized by 1-fluoro-2,4-dinitrobenzene (DNFB). Results: We found that T cell-specific deletio
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