| First Author | Owens BM | Year | 2012 |
| Journal | PLoS Pathog | Volume | 8 |
| Issue | 7 | Pages | e1002827 |
| PubMed ID | 22911108 | Mgi Jnum | J:195372 |
| Mgi Id | MGI:5478680 | Doi | 10.1371/journal.ppat.1002827 |
| Citation | Owens BM, et al. (2012) IL-10-producing Th1 cells and disease progression are regulated by distinct CD11c(+) cell populations during visceral leishmaniasis. PLoS Pathog 8(7):e1002827 |
| abstractText | IL-10 is a critical regulatory cytokine involved in the pathogenesis of visceral leishmaniasis caused by Leishmania donovani and clinical and experimental data indicate that disease progression is associated with expanded numbers of CD4(+) IFNgamma(+) T cells committed to IL-10 production. Here, combining conditional cell-specific depletion with adoptive transfer, we demonstrate that only conventional CD11c(hi) DCs that produce both IL-10 and IL-27 are capable of inducing IL-10-producing Th1 cells in vivo. In contrast, CD11c(hi) as well as CD11c(int/lo) cells isolated from infected mice were capable of reversing the host protective effect of diphtheria toxin-mediated CD11c(+) cell depletion. This was reflected by increased splenomegaly, inhibition of NO production and increased parasite burden. Thus during chronic infection, multiple CD11c(+) cell populations can actively suppress host resistance and enhance immunopathology, through mechanisms that do not necessarily involve IL-10-producing Th1 cells. |
