| First Author | Hayashi Y | Year | 1996 |
| Journal | Autoimmunity | Volume | 23 |
| Issue | 4 | Pages | 269-77 |
| PubMed ID | 8915033 | Mgi Jnum | J:36643 |
| Mgi Id | MGI:84071 | Doi | 10.3109/08916939608995349 |
| Citation | Hayashi Y, et al. (1996) Cytokine gene expression and autoantibody production in Sjogren's syndrome of MRL/lpr mice. Autoimmunity 23(4):269-77 |
| abstractText | In an attempt to elucidate the mechanism of development of organ-specific autoimmune lesions resembling human Sjogren's syndrome of MRL/lpr mice, we have analyzed local cytokine gene expressions and organ-specific autoantibody production in vivo. We have demonstrated that a major proportion of T cells bearing CD4 and V(beta)8 molecules are essentially responsible for triggering the autoimmunity in the salivary glands of MRL/lpr mice. The local cytokine gene expressions including interferon(IFN)-gamma, IL-12(p40) mRNAs were observed during the course of murine Sjogren's syndrome in MRL/lpr autoimmune strain. In particular, a high level of local expressions of IL-12 mRNA was detected earlier in the proinflammatory stage of autoimmune lesions. A significant level of local expression of MHC class-II(I-Ak) mRNA was detected before the onset of inflammatory lesions in the salivary glands, and I-Ak-positive epithelial duct cells were frequently observed in the salivary glands of MRL/lpr mice. In addition, we found the salivary gland-specific autoantibody in sera from MRL/lpr mice with early phase of autoimmune lesions by immunoblot analysis. These results suggest that cytokine gene stimulation and autoantibody production are essentially involved in the development of organ-specific autoimmune lesions in Sjogren's syndrome of MRL/lpr mice. |
