| First Author | McBerry C | Year | 2014 |
| Journal | Eur J Immunol | Volume | 44 |
| Issue | 2 | Pages | 469-79 |
| PubMed ID | 24165808 | Mgi Jnum | J:208723 |
| Mgi Id | MGI:5564867 | Doi | 10.1002/eji.201343658 |
| Citation | McBerry C, et al. (2014) PD-1 modulates steady-state and infection-induced IL-10 production in vivo. Eur J Immunol 44(2):469-79 |
| abstractText | Programmed death-1 (PD-1) plays an important role in mediating immune tolerance through mechanisms that remain unclear. Herein, we investigated whether PD-1 prevents excessive host tissue damage during infection with the protozoan parasite, Toxoplasma gondii. Surprisingly, our results demonstrate that PD-1-deficient mice have increased susceptibility to T. gondii, with increased parasite cyst counts along with reduced type-1 cytokine responses (IL-12 and IFN-gamma). PD-1(-)/(-) DCs showed no cell intrinsic defect in IL-12 production in vitro. Instead, PD-1 neutralization via genetic or pharmacological approaches resulted in a striking increase in IL-10 release, which impaired type-1-inflammation during infection. Our results indicate that the absence of PD-1 increases IL-10 production even in the absence of infection. Although the possibility that such increased IL-10 protects against autoimmune damage is speculative, our results show that IL-10 suppresses the development of protective Th1 immune response after T. gondii infection. |
