Allergic dermatitis (AD) clinically presents with skin erythematous plaques, eruption, and elevated serum IgE, and T helper cell type 2 and 1 (Th2 and Th1) cytokine levels. Dinitrochlorobenzene (DNCB)-induced contact hypersensitivity of the skin is a commonly-used mice model for studying the pathogenesis of allergic dermatitis. IK cytokine is known to suppress IFN-γ induced expression of MHC class II molecules on B cells by increasing cAMP. Recently, we reported that truncated IK (tIK) cytokine-expressed transgenic (Tg) mouse are less susceptible to inflammatory arthritis and tIK overexpression suppresses the differentiation of TH1 and TH17 cells and the activation of macrophages. However, there are still limited studies showing the functionality of this cytokine in inflammatory diseases such as AD. Here, we investigated whether tIK cytokine expressing Tg mice are less susceptible for DNCB induced AD. DNCB treatment caused severe dermatitis symptoms in wild type (WT) including weight loss, increased ear thickness and scratching behavior but those symptoms are significantly reduced in tIK Tg mice. The weights of draining lymph node (dLN) and spleen were also much less in tIKTg mice. In addition, tIK overexpression decreased IgE serum level, mRNA transcript of mast cell associated factors in Tg mice compared to WT mice. Analyzing T cell subpopulation in dLN revealed that Th2 and Th17 cell differentiation were suppressed by tIK expression while Tregs and Th1 differentiation were not affected. Taken together, our results presented here suggest that tIK expression effectively attenuate DNCB induced allergic contact dermatitis lesions by modulation Th cell differentiation. Futher studies are needed to elucidate immunological and molecular mechanisms by which tIK functions on this disease model.