NK cells and conventional dendritic cells engage in reciprocal activation for the induction of inflammatory responses during Plasmodium berghei ANKA infection
Details
Publication Year 2013-02,Volume 218,Issue #2,Page 263-271
Journal Title
IMMUNOBIOLOGY
Publication Type
Journal Article
Abstract
Cerebral malaria (CM) is the most severe syndrome associated with Plasmodium falciparum infections. Experimental evidence suggests that disease results from the sequestration of parasitized-red blood cells (pRBCs) together with inflammatory leukocytes within brain capillaries. We have previously shown that NK cells stimulate migration of CXCR3(+) T cells to the brain of Plasmodium berghei ANKA-infected mice. Here we investigated whether interactions between NK cells and dendritic cells (DCs) are required for the induction of T cell responses involved in disease. For that, NK cell-depleted and control mice were infected with transgenic parasites expressing model T cell epitopes. T cells from TCR transgenic mice specific for those epitopes were adoptively transferred and proliferation was determined. NK cell depletion significantly reduced CD8(+) but not CD4(+) DC-mediated T cell priming. Lack of NK cells did not compromise CD8(+) T cell responses in IL-12(-/-) mice, suggesting that NK cells stimulate IL-12 output by DCs required for optimal T cell priming. The contribution of DCs to NK cell function was also investigated. DC depletion and genetic deletion of IL-12 dramatically reduced NK cell-mediated IFN-gamma responses to malaria. Thus NK cells and DCs engage in reciprocal activation for the induction of inflammatory responses involved in severe malaria. (C) 2012 Elsevier GmbH. All rights reserved.
Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
Keywords
MURINE CEREBRAL MALARIA; TUMOR-NECROSIS-FACTOR; NATURAL-KILLER-CELLS; FALCIPARUM-MALARIA; T-CELLS; INTERFERON-GAMMA; GENE-COMPLEX; CROSS-TALK; IFN-GAMMA; PATHOGENESIS
Research Division(s)
Infection And Immunity
Terms of Use/Rights Notice
Copyright © 2012 Elsevier GmbH. All rights reserved.


Creation Date: 2013-02-01 12:00:00
An error has occurred. This application may no longer respond until reloaded. Reload 🗙