| First Author | Ing R | Year | 2009 |
| Journal | Infect Immun | Volume | 77 |
| Issue | 2 | Pages | 770-82 |
| PubMed ID | 19015248 | Mgi Jnum | J:143758 |
| Mgi Id | MGI:3828907 | Doi | 10.1128/IAI.00994-08 |
| Citation | Ing R, et al. (2009) Dendritic cell and NK cell reciprocal cross talk promotes gamma interferon-dependent immunity to blood-stage Plasmodium chabaudi AS infection in mice. Infect Immun 77(2):770-82 |
| abstractText | Dendritic cells (DCs) are important accessory cells for promoting NK cell gamma interferon (IFN-gamma) production in vitro in response to Plasmodium falciparum-infected red blood cells (iRBC). We investigated the requirements for reciprocal activation of DCs and NK cells leading to Th1-type innate and adaptive immunity to P. chabaudi AS infection. During the first week of infection, the uptake of iRBC by splenic CD11c(+) DCs in resistant wild-type (WT) C57BL/6 mice was similar to that in interleukin 15(-/-) (IL-15(-/-)) and IL-12p40(-/-) mice, which differ in the severity of P. chabaudi AS infection. DCs from infected IL-15(-/-) mice expressed costimulatory molecules, produced IL-12, and promoted IFN-gamma secretion by WT NK cells in vitro as efficiently as WT DCs. In contrast, DCs from infected IL-12p40(-/-) mice exhibited alterations in maturation and cytokine production and were unable to induce NK cell IFN-gamma production. Coculture of DCs and NK cells demonstrated that DC-mediated NK cell activation required IL-12 and, to a lesser extent, IL-2, as well as cell-cell contact. In turn, NK cells from infected WT mice enhanced DC maturation, IL-12 production, and priming of CD4(+) T-cell proliferation and IFN-gamma secretion. Infected WT mice depleted of NK cells, which exhibit increased parasitemia, had impaired DC maturation and DC-induced CD4(+) Th1 cell priming. These findings indicate that DC-NK cell reciprocal cross talk is critical for control and rapid resolution of P. chabaudi AS infection and provide in vivo evidence for the importance of this interaction in IFN-gamma-dependent immunity to malaria. |
