| First Author | Takahashi M | Year | 1996 |
| Journal | Cell Immunol | Volume | 170 |
| Issue | 1 | Pages | 54-62 |
| PubMed ID | 8660799 | Mgi Jnum | J:33222 |
| Mgi Id | MGI:80702 | Doi | 10.1006/cimm.1996.0133 |
| Citation | Takahashi M, et al. (1996) Mechanism of the development of autoimmune dacryodenitis in the mouse model for primary Sjogren's syndrome. Cell Immunol 170(1):54-62 |
| abstractText | To elucidate the mechanism of development in autoimmune lacrimal gland disease, we analyzed different aspects of autoimmune dacryoadenitis in a newly established mouse model for primary Sjogren's syndrome, focusing on the local expressions of cytokine genes, and the repertoire of T cell receptor (TCR) V beta genes transcribed within the inflammatory infiltration in the lacrimal glands. We found that the vast majority of inflammatory infiltration into the lacrimal glands were CD4+ V beta 8+ T cells. We detected the up-regulation of local cytokine genes (IL-1 beta, TNF-alpha, IL-2, IFN-gamma, IL-10, IL-12p40) in the lacrimal glands with very early inflammatory lesions by reverse transcriptase (RT)-PCR analysis. The predominant expression of the V beta 8 gene segment was detected from a very early stage, while extensive age-related diversity of TCR V beta gene usage was observed. Single-strand conformation polymorphism (SSCP) analysis demonstrated a distinct and a common binding pattern in the PCR product of the V beta 8 gene on the infiltrating cells during the course of the disease. These data suggest that in autoimmune dacryoadenitis of the mouse model for primary Sjogren's syndrome there may be a restricted usage of TCR V beta elements on a very early stage of the autoimmune lesion to recognize unknown self-antigen, and the autoreactive CD4+ T cells constitute a unique cytokine profile in the autoimmune lacrimal gland disease. |
