| First Author | Zaheer M | Year | 2018 |
| Journal | J Autoimmun | Volume | 93 |
| Pages | 45-56 | PubMed ID | 29934134 |
| Mgi Jnum | J:315611 | Mgi Id | MGI:6829392 |
| Doi | 10.1016/j.jaut.2018.06.004 | Citation | Zaheer M, et al. (2018) Protective role of commensal bacteria in Sjogren Syndrome. J Autoimmun 93:45-56 |
| abstractText | CD25 knock-out (CD25KO) mice spontaneously develop Sjogren Syndrome (SS)-like inflammation. We investigated the role of commensal bacteria by comparing CD25KO mice housed in conventional or germ-free conditions. Germ-free CD25KO mice have greater corneal barrier dysfunction, lower goblet cell density, increased total lymphocytic infiltration score, increased expression of IFN-gamma, IL-12 and higher a frequency of CD4(+)IFN-gamma(+) cells than conventional mice. CD4(+) T cells isolated from female germ-free CD25KO mice adoptively transferred to naive immunodeficient RAG1KO recipients caused more severe Sjogren-like disease than CD4(+) T cells transferred from conventional CD25KO mice. Fecal transplant in germ-free CD25KO mice reversed the spontaneous dry eye phenotype and decreased the generation of pathogenic CD4(+)IFN-gamma(+) cells. Our studies indicate that lack of commensal bacteria accelerates the onset and severity of dacryoadenitis and generates autoreactive CD4(+)T cells with greater pathogenicity in the CD25KO model, suggesting that the commensal bacteria or their metabolites products have immunoregulatory properties that protect exocrine glands in the CD25KO SS model. |
