The existence of helper-T cell (Th) subsets, types I and II (Th1/Th2), provides a framework for understanding pathological immune responses. We previously reported that a benzoimidazole derivative,
M50367, acted directly on naive Th cells to inhibit their differentiation into Th2 cells. Oral treatment with this compound reduced the Th2 response in vivo and suppressed
disease progression in a murine model of atopic
asthma. In this study, we investigated the effect of
M50367 on 2 other murine disease models, such as
atopic dermatitis and intradermal
tumor-bearing mice, the pathogenesis of which may be related to the Th2 response. NC/Nga mice treated with a repeated application of
picryl chloride developed
atopic dermatitis-like skin lesions together with
IgE hyper-production.
M50367 (30 mg/kg) significantly inhibited the
IgE hyper-production without affecting the skin lesions. In C57BL/6 mice bearing intradermal B16F10
melanoma,
M50367 (30, 100 mg/kg) significantly inhibited
splenomegaly and enhanced spontaneous
interferon-gamma release from cultured splenocytes in a dose-dependent manner, though its effect on
tumor volume was limited. These results suggest that
M50367 could reduce the Th2 response (
IgE hyper-production) and enhance the Th1 response (splenocytes
interferon-gamma production) in these models. In contrast to previous results in the
asthma model, its
immunomodulation did not lead to the suppression of
disease progression, indicating that the pathogenesis of these models might not simply depend on Th2 response.