| First Author | Sonoda KH | Year | 1999 |
| Journal | J Exp Med | Volume | 190 |
| Issue | 9 | Pages | 1215-26 |
| PubMed ID | 10544194 | Mgi Jnum | J:58315 |
| Mgi Id | MGI:1347204 | Doi | 10.1084/jem.190.9.1215 |
| Citation | Sonoda KH, et al. (1999) CD1-reactive natural killer T cells are required for development of systemic tolerance through an immune-privileged site [see comments]. J Exp Med 190(9):1215-26 |
| abstractText | Systemic tolerance can be elicited by introducing antigen into an immune-privileged site, such as the eye, or directly into the blood. Both routes of immunization result in a selective deficiency of systemic delayed type hypersensitivity. Although the experimental animal model of anterior chamber-associated immune deviation (ACAID) occurs in most mouse strains, ACAID cannot be induced in several mutant mouse strains that are coincidentally deficient in natural killer T (NKT) cells. Therefore, this model for immune-privileged site-mediated tolerance provided us with an excellent format for studying the role of NKT cells in the development of tolerance. The following data show that CD1-reactive NKT cells are required for the development of systemic tolerance induced via the eye as follows: (a) CD1 knockout mice were unable to develop ACAID unless they were reconstituted with NKT cells together with CD1(+) antigen-presenting cells; (b) specific antibody depletion of NKT cells in vivo abrogated the development of ACAID; and (c) anti-CD1 monoclonal antibody treatment of wild-type mice prevented ACAID development. Significantly, CD1-reactive NKT cells were not required for intravenously induced systemic tolerance, thereby establishing that different mechanisms mediate development of tolerance to antigens inoculated by these routes. A critical role for NKT cells in the development of systemic tolerance associated with an immune-privileged site suggests a mechanism involving NKT cells in self-tolerance and their defects in autoimmunity. |
