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      Limited response of NK92 cells to Plasmodium falciparum-infected erythrocytes

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          Abstract

          Background

          Mechanisms by which anti-malarial immune responses occur are still not fully clear. Natural killer (NK) cells are thought to play a pivotal role in innate responses against Plasmodium falciparum. In this study, the suitability of NK92 cells as models for the NK mechanisms involved in the immune response against malaria was investigated.

          Methods

          NK92 cells were assessed for several signs of activation and cytotoxicity due to contact to parasites and were as well examined by oligonucleotide microarrays for an insight on the impact P. falciparum-infected erythrocytes have on their transcriptome. To address the parasite side of such interaction, growth inhibition assays were performed including non-NK cells as controls.

          Results

          By performing microarrays with NK92 cells, the impact of parasites on a transcriptional level was observed. The findings show that, although not evidently activated by iRBCs, NK92 cells show transcriptional signs of priming and proliferation. In addition, decreased parasitaemia was observed due to co-incubation with NK92 cells. However, such effect might not be NK-specific since irrelevant cells also affected parasite growth in vitro.

          Conclusions

          Although NK92 cells are here shown to behave as poor models for the NK immune response against parasites, the results obtained in this study may be of use for future investigations regarding host-parasites interactions in malaria.

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          Most cited references23

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          Adherence of Plasmodium falciparum to chondroitin sulfate A in the human placenta.

          Women are particularly susceptible to malaria during first and second pregnancies, even though they may have developed immunity over years of residence in endemic areas. Plasmodium falciparum-infected red blood cells (IRBCs) were obtained from human placentas. These IRBCs bound to purified chondroitin sulfate A (CSA) but not to other extracellular matrix proteins or to other known IRBC receptors. IRBCs from nonpregnant donors did not bind to CSA. Placental IRBCs adhered to sections of fresh-frozen human placenta with an anatomic distribution similar to that of naturally infected placentas, and this adhesion was competitively inhibited by purified CSA. Thus, adhesion to CSA appears to select for a subpopulation of parasites that causes maternal malaria.
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            Human malaria parasites in continuous culture. 1976.

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              Cross-talk between activated human NK cells and CD4+ T cells via OX40-OX40 ligand interactions.

              It is important to understand which molecules are relevant for linking innate and adaptive immune cells. In this study, we show that OX40 ligand is selectively induced on IL-2, IL-12, or IL-15-activated human NK cells following stimulation through NKG2D, the low affinity receptor for IgG (CD16) or killer cell Ig-like receptor 2DS2. CD16-activated NK cells costimulate TCR-induced proliferation, and IFN-gamma produced by autologous CD4+ T cells and this process is dependent upon expression of OX40 ligand and B7 by the activated NK cells. These findings suggest a novel and unexpected link between the natural and specific immune responses, providing direct evidence for cross-talk between human CD4+ T cells and NK receptor-activated NK cells. Copyright 2004 The American Association of Immunologists, Inc.
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                Author and article information

                Journal
                Malar J
                Malaria Journal
                BioMed Central
                1475-2875
                2011
                21 October 2011
                : 10
                : 311
                Affiliations
                [1 ]Institute for Tropical Medicine, Tübingen University, Wilhelmstrasse, 27; 72074 Tübingen; Germany
                Article
                1475-2875-10-311
                10.1186/1475-2875-10-311
                3213193
                22018162
                c7b705f2-e0ae-4543-8d91-61891dda60ef
                Copyright ©2011 de Carvalho et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 7 July 2011
                : 21 October 2011
                Categories
                Research

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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