| First Author | Skarstein K | Year | 1997 |
| Journal | Clin Immunol Immunopathol | Volume | 84 |
| Issue | 2 | Pages | 177-84 |
| PubMed ID | 9245550 | Mgi Jnum | J:42117 |
| Mgi Id | MGI:1095203 | Doi | 10.1006/clin.1997.4387 |
| Citation | Skarstein K, et al. (1997) Effects of sialadenitis after cellular transfer in autoimmune MRL/lpr mice. Clin Immunol Immunopathol 84(2):177-84 |
| abstractText | The MRL/Mp mice bearing a lymphoproliferative gene, lpr (MRL/Mp-lpr/lpr), provide an appropriate model for the study of autoimmune mechanisms leading to the destruction of salivary and lacrimal gland tissue in Sjogren's syndrome. By 7-8 weeks of age, progressive focal inflammatory cell infiltrates are observed in salivary glands. We examined the possibility of transferring this disorder into syngeneic, young animals. Spleen cells and infiltrating mononuclear cells (MNC) enzymatically eluted from salivary glands were used. The results showed that sialadenitis could be transferred in vivo to young MRL/lpr mice by splenic and salivary gland MNC. The most striking finding was observed in male recipients where the highest incidence of sialadenitis (5/5) was seen in the group injected intravenously with a small dose (1 x 10(6) of salivary gland MNC, CD8+ splenic cells alone were not able to transfer disease. On the other hand, CD4+ splenic cells induced a more severe sialadenitis compared to the control animals. The transfer of pooled cells from salivary glands resulted in the most severe and accelerating sialadenitis (P < 0.05) in female recipients compared with the control animals. Overall, the highest sialadenitis scores (> 0.10) were obtained only after transfer of CD4+ spleen cells and infiltrating salivary gland MNC. These findings indicate that sialadenitis in MRL/lpr mice is mediated by cellular mechanisms and suggest that the infiltrating MNC have the ability to accelerate autoimmune disease in the salivary glands. |
