| First Author | Van Belle TL | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 6 | Pages | 2915-22 |
| PubMed ID | 21832162 | Mgi Jnum | J:179258 |
| Mgi Id | MGI:5301512 | Doi | 10.4049/jimmunol.1000180 |
| Citation | Van Belle TL, et al. (2011) Development of autoimmune diabetes in the absence of detectable IL-17A in a CD8-driven virally induced model. J Immunol 187(6):2915-22 |
| abstractText | Recent studies have shown that IL-17 can contribute beneficially to pathogen defense but also that excessive IL-17 levels are associated with chronic inflammation and autoimmune disorders. To date, the role of IL-17 in viral infections and type 1 diabetes is ambiguous. In this study, we used IL-17A enhanced green fluorescent protein bicistronic reporter mouse strains to analyze in situ production of IL-17A. Upon Klebsiella pneumoniae bacterial infection, CD4(+) and gammadelta T cells produce IL-17A. In contrast, CD4(+) or CD8(+) T cells do not produce IL-17A in response to acute or protracted viral infection with lymphocytic choriomeningitis virus or during autoimmune diabetes development in the CD8-driven lymphocytic choriomeningitis virus-induced model of type 1 diabetes. We conclude that viral elimination and type 1 diabetes can occur in the absence of detectable IL-17A production, suggesting IL-17A is not essential in these settings. |
