| First Author | Lee IF | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 6 | Pages | 2898-904 |
| PubMed ID | 21844383 | Mgi Jnum | J:179247 |
| Mgi Id | MGI:5301501 | Doi | 10.4049/jimmunol.1002551 |
| Citation | Lee IF, et al. (2011) NKT cells are required for complete Freund's adjuvant-mediated protection from autoimmune diabetes. J Immunol 187(6):2898-904 |
| abstractText | Autoimmune diabetes in NOD mice can be prevented by application of Ags derived from Mycobacterium tuberculosis in the form of bacillus Calmette-Guerin or CFA. Disease protection by CFA is associated with a reduction in the numbers of pathogenic beta-cell specific, self-reactive CTLs, a phenomenon dependent on the presence and function of NK cells. However, the mechanisms by which NK cells are activated and recruited by heat-killed M. tuberculosis within CFA are unclear. In this study, we report that CFA-mediated NK cell activation and mobilization is dependent on CD1d expression. The administration of M. tuberculosis from CFA results in rapid NKT cell activation and IFN-gamma secretion both in vitro and in vivo. CFA-induced NKT cell activation is intact in MyD88(-/-) mice suggesting that the mechanism is independent of TLR signaling. Furthermore, CD1d expression was found to be essential for both M. tuberculosis-triggered NKT cell activation and CFA-mediated protection of NOD mice from diabetes. Collectively, these findings reveal hitherto previously unidentified roles for NKT cells in the adjuvant-promoting effects of CFA on innate and adaptive immunity. |
