| First Author | Tsuji-Yamada J | Year | 2001 |
| Journal | Biochem Biophys Res Commun | Volume | 280 |
| Issue | 3 | Pages | 707-12 |
| PubMed ID | 11162578 | Mgi Jnum | J:67087 |
| Mgi Id | MGI:1929829 | Doi | 10.1006/bbrc.2000.4171 |
| Citation | Tsuji-Yamada J, et al. (2001) Effect of IL-12 encoding plasmid administration on tight-skin mouse. Biochem Biophys Res Commun 280(3):707-12 |
| abstractText | The tight-skin (Tsk/+) mutant mice, a putative murine model of scleroderma, are characterized by the excessive deposition of collagen and the presence of antinuclear antibodies. Type 2 cytokines, such as IL-4 and IL-6, are capable of regulating the synthesis of various matrix molecules, including type I collagen, by fibroblasts. IL-12 is well known to induce type 1 cytokine production and to reduce type 2 activity. Here, we examined the effect of IL-12 encoding plasmid (pCAGGSIL-12) on the disease progression of Tsk/+ mice. pCAGGSIL-12 plasmid or pCAGGS parental vector was injected intramuscularly 7 times at 3 week intervals into Tsk/+ mice. One week after the last injection, pCAGGSIL-12 administered Tsk/+ mice exhibited a marked decrease in the skin thickness compared with the mice treated with pCAGGS vector. The serum levels of antinuclear antibodies were diminished in pCAGGSIL-12 treated mice. IL-4 production by spleen cells from pCAGGSIL-12 plasmid treated mice was significantly lower than that from vector treated mice. These results indicate that pCAGGSIL-12 administration into Tsk/+ mice had beneficial effects in preventing the collagen accumulation in the skin and suppressing the autoimmunity via improvement of Th1/Th2 balance. The present study suggests that the IL-12 encoding plasmid administration might have a therapeutic effect on systemic sclerosis. Copyright 2001 Academic Press. |
