| First Author | Ejrnaes M | Year | 2006 |
| Journal | J Exp Med | Volume | 203 |
| Issue | 11 | Pages | 2461-72 |
| PubMed ID | 17030951 | Mgi Jnum | J:124631 |
| Mgi Id | MGI:3722049 | Doi | 10.1084/jem.20061462 |
| Citation | Ejrnaes M, et al. (2006) Resolution of a chronic viral infection after interleukin-10 receptor blockade. J Exp Med 203(11):2461-72 |
| abstractText | A defining characteristic of persistent viral infections is the loss and functional inactivation of antiviral effector T cells, which prevents viral clearance. Interleukin-10 (IL-10) suppresses cellular immune responses by modulating the function of T cells and antigen-presenting cells. In this paper, we report that IL-10 production is drastically increased in mice persistently infected with lymphocytic choriomeningitis virus. In vivo blockade of the IL-10 receptor (IL-10R) with a neutralizing antibody resulted in rapid resolution of the persistent infection. IL-10 secretion was diminished and interferon gamma production by antiviral CD8+ T cells was enhanced. In persistently infected mice, CD8alpha+ dendritic cell (DC) numbers declined early after infection, whereas CD8alpha- DC numbers were not affected. CD8alpha- DCs supported IL-10 production and subsequent dampening of antiviral T cell responses. Therapeutic IL-10R blockade broke the cycle of IL-10-mediated immune suppression, preventing IL-10 priming by CD8alpha- DCs and enhancing antiviral responses and thereby resolving infection without causing immunopathology. |
