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Inability of IL-12 to Down-Regulate IgE Synthesis Due to Defective Production of IFN- in Atopic NC/Nga Mice¹

Masahiro Matsumoto^*,, Atsuko Itakura^*, Akane Tanaka^*, Chie Fujisawa^* and Hiroshi Matsuda^2,*

^* Laboratory of Clinical Immunology, Department of Veterinary Clinic, Faculty of Agriculture, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan; and Department of Pathology, Toxicology Research Laboratories, Fujisawa Pharmaceutical, Osaka, Japan

NC/Nga mice raised in nonsterile circumstances spontaneously suffer from atopic dermatitis-like skin lesions with IgE hyperproduction. We investigated effects of rIL-12 on the IgE production in NC/Nga mice. rIL-12 administration was successful to suppress the increase of IgE levels in BALB/c mice immunized with OVA and aluminum hydroxide, but failed to abrogate that in NC/Nga mice. Both in vivo and in vitro IFN- production induced by rIL-12 was less in NC/Nga mice than in BALB/c mice. Addition of rIFN- to rIL-4 and LPS completely abrogated IgE production by B cells of BALB/c mice, but was insufficient to suppress it by B cells of NC/Nga mice. In splenic cells pretreated with Con A, STAT4 was phosphorylated at the tyrosine residue by addition of rIL-12, which was more weakly inducible in NC/Nga mice than in BALB/c mice. Finally, we examined the preventive ability of rIL-12 on the clinical aspects of atopic dermatitis in NC/Nga mice. rIL-12 administration resulted in exacerbation of development of the skin lesions and IgE production in NC/Nga mice raised in nonsterile circumstances. These results suggest that defective production of IFN- by T cells less sensitive to IL-12 and low responsiveness of B cells to IFN- may contribute to IgE hyperproduction in NC/Nga mice, and that IL-12 may have no ability to improve the clinical aspects of NC/Nga mice.

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