1. To study the role of
interleukin (IL)-4 in the onset of
contact hypersensitivity (CH) in mice, the effect of
IL-4 gene-depletion and anti-IL-4
monoclonal antibody treatment on
dinitrofluorobenzene (
DNFB)-induced CH was examined. Simultaneously, to clarify the effect of background gene,
DNFB-induced CH in BALB/c and C57BL/6 mice was compared. 2. Five repeated topical applications of
DNFB to the ears of mice resulted in CH of the ears in terms of increases in ear thickness and histopathological changes. The magnitude of ear thickness increase in BALB/c mice was almost three times greater than that in C57BL/6 mice. 3. The CH in BALB/c mice was significantly suppressed by
IL-4 gene-depletion and anti-IL-4
monoclonal antibody treatment. In contrast, the symptoms of
dermatitis in C57BL/6 mice were slightly affected by the same treatment. These changes corresponded well to the production of specific
IgE antibody. 4. Total
IgE antibody production and the expression of productive Cepsilon
mRNA were dramatically suppressed by
IL-4 gene-depletion and anti-IL-4 treatment in BALB/c and C57BL/6 mice. Neither total
IgG nor
IgM levels in either strain of mice was altered by depletion of
IL-4. 5. The expression of IFN-gamma in the skin lesion was dramatically suppressed by
IL-4 gene-depletion in BALB/c mice, but not in C57BL/6 mice. 6. These findings indicate that
IL-4 plays an important role in the onset of
DNFB-induced CH in BALB/c mice, but not in C57BL/6 mice.