EFFECTS ON SIALADENITIS AFTER CELLULAR TRANSFER IN AUTOIMMUNE MRL LPRMICE/

Citation
K. Skarstein et al., EFFECTS ON SIALADENITIS AFTER CELLULAR TRANSFER IN AUTOIMMUNE MRL LPRMICE/, Clinical immunology and immunopathology, 84(2), 1997, pp. 177-184
Citations number
21
Categorie Soggetti
Pathology,Immunology
ISSN journal
00901229
Volume
84
Issue
2
Year of publication
1997
Pages
177 - 184
Database
ISI
SICI code
0090-1229(1997)84:2<177:EOSACT>2.0.ZU;2-9
Abstract
The MRL/Mp mice bearing a lymphoproliferative gene, lpr (MRL/Mp-lpr/lp r), provide an appropriate model for the study of autoimmune mechanism s leading to the destruction of salivary and lacrimal gland tissue in Sjogren's syndrome. By 7-8 weeks of age, progressive focal inflammator y cell infiltrates are observed in salivary glands. We examined the po ssibility of transferring this disorder into syngeneic, young animals. Spleen cells and infiltrating mononuclear cells (MNC) enzymatically e luted from salivary glands were used. The results showed that sialaden itis could be transferred in vine to young MRL/lpr mice by splenic and salivary gland MNC. The most striking finding was observed in male re cipients where the highest incidence of sialadenitis (5/5) was seen in the group injected intravenously with a small dose (1 x 10(6)) of sal ivary 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 acceleratin g sialadenitis (P < 0.05) in female recipients compared with the contr ol animals. Overall, the highest sialadenitis scores (>0.10) were obta ined only after transfer of CD4(+) spleen cells and infiltrating saliv ary gland MNC. These findings indicate that sialadenitis in MRL/lpr mi ce is mediated by cellular mechanisms and suggest that the infiltratin g MNC have the ability to accelerate autoimmune disease in the salivar y glands. a 1997 Academic Press.