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Baratin, M.* ; Roetynck, S.* ; Lépolard, C.* ; Falk, C. ; Sawadogo, S.* ; Uematsu, S.* ; Akira, S.* ; Ryffel, B.* ; Tiraby, J.-G.* ; Alexopoulou, L.* ; Kirschning, C.J.*

Natural killer cell and macrophage cooperation in MyD88-dependent innate responses to Plasmodium falciparum.

Proc. Natl. Acad. Sci. U.S.A. 102, 14747-14752 (2005)
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IFN-gamma secretion by natural killer (NK) cells is pivotal to several tumor and viral immune responses, during which NK and dendritic cells cooperation is required. We show here that macrophages are mandatory for NK cell IFN-gamma secretion in response to erythrocytes infected with Plasmodium falciparum (Pf), a causative agent of human malaria. In addition, direct sensing of Pf infection by NK cells induces their production of the proinflammatory chemokine CXCL8, without triggering their granule-mediated cytolytic programs. Despite their reported role in Pf recognition, Toll-like receptor (TLR) 2, TLR9, and TLR11 are individually dispensable for NK cell activation induced by Pf-infected erythrocytes. However, IL-18R expression on NK cells, IL-18 production by macrophages, and MyD88 on both cell types are essential components of this previously undescribed pathway of NK cell activation in response to a parasite infection.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter innate immunity; HUMAN NK CELLS; DENDRITIC CELLS; INFECTED ERYTHROCYTES; IMMUNE-RESPONSE; PROINFLAMMATORY RESPONSES; MALARIA; RECEPTOR; INDUCTION; ACTIVATION; GLYCOSYLPHOSPHATIDYLINOSITOLS
Sprache englisch
Veröffentlichungsjahr 2005
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Zeitschrift Proceedings of the National Academy of Sciences of the United States of America
Quellenangaben Band: 102, Heft: 41, Seiten: 14747-14752 Artikelnummer: , Supplement: ,
Verlag National Academy of Sciences
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Immunology (IMI)
POF Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Immune Response and Infection
PSP-Element(e) G-501700-006
PubMed ID 16203971
DOI 10.1073/pnas.0507355102
WOS ID 000232603600049
Erfassungsdatum 2005-12-14
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