| First Author | Najafian N | Year | 2003 |
| Journal | J Clin Invest | Volume | 112 |
| Issue | 7 | Pages | 1037-48 |
| PubMed ID | 14523041 | Mgi Jnum | J:85805 |
| Mgi Id | MGI:2677077 | Doi | 10.1172/JCI17935 |
| Citation | Najafian N, et al. (2003) Regulatory functions of CD8+CD28- T cells in an autoimmune disease model. J Clin Invest 112(7):1037-48 |
| abstractText | CD8+ T cell depletion renders CD28-deficient mice susceptible to experimental autoimmune encephalomyelitis (EAE). In addition, CD8-/-CD28-/- double-knockout mice are susceptible to EAE. These findings suggest a role for CD8+ T cells in the resistance of CD28-deficient mice to disease. Adoptive transfer of CD8+CD28- T cells into CD8-/- mice results in significant suppression of disease, while CD8+CD28+ T cells demonstrate no similar effect on the clinical course of EAE in the same recipients. In vitro, CD8+CD28- but not CD8+CD28+ T cells suppress IFN-gamma production of myelin oligodendrocyte glycoprotein-specific CD4+ T cells. This suppression requires cell-to-cell contact and is dependent on the presence of APCs. APCs cocultured with CD8+CD28- T cells become less efficient in inducing a T cell-dependent immune response. Such interaction prevents upregulation of costimulatory molecules by APCs, hence decreasing the delivery of these signals to CD4+ T cells. These are the first data establishing that regulatory CD8+CD28- T cells occur in normal mice and play a critical role in disease resistance in CD28-/- animals. |
