| First Author | Habu Y | Year | 2001 |
| Journal | J Immunol | Volume | 166 |
| Issue | 9 | Pages | 5439-47 |
| PubMed ID | 11313381 | Mgi Jnum | J:69053 |
| Mgi Id | MGI:1933940 | Doi | 10.4049/jimmunol.166.9.5439 |
| Citation | Habu Y, et al. (2001) The Mechanism of a Defective IFN-gamma Response to Bacterial Toxins in an Atopic Dermatitis Model, NC/Nga Mice, and the Therapeutic Effect of IFN-gamma, IL-12, or IL-18 on Dermatitis. J Immunol 166(9):5439-47 |
| abstractText | NC/Nga (NC) mice raised under conventional conditions (CONV: NC mice) spontaneously develop dermatitis similar to human atopic dermatitis, whereas NC mice raised under the specific pathogen-free conditions do not develop dermatitis. In the present study, we show that the representative Th1 cytokine, IFN-gamma levels in the sera of NC mice, injected with either staphylococcal enterotoxin B or endotoxin (LPS), to be severalfold lower than those of normal mice. The low IFN-gamma response to staphylococcal enterotoxin B was correlated to the lack of regular Vbeta8(+) T cells and Vbeta8(+) NK T cells, and the low IFN-gamma response to LPS was correlated to an impaired IL-18 production of macrophages. The CD3-stimulated IL-4 production from liver and spleen T cells from CONV: NC mice in vitro was greatly augmented. The serum IL-4 levels of untreated CONV: NC mice also were higher than those of normal mice and specific pathogen-free NC mice. Treatment of CONV: NC mice either with IFN-gamma, IL-12, or IL-18 twice a week from 4 wk of age substantially inhibited the elevation of the serum IgE levels, serum IL-4 levels, and dermatitis, and IL-12 or IL-18 treatment also reduced the in vitro IL-4 production from CD3-stimulated liver T cells. The systemic deficiency in the Th1 response to bacterial stimulation thus leads to a Th2-dominant state and may induce an abnormal cellular immune response in the skin accompanied with an overproduction of IgE and a susceptibility to dermatitis in NC mice. |
