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Kriegeskorte, A.K.* ; Gebhardt, F.E.* ; Porcellini, S.* ; Schiemann, M. ; Stemberger, C.* ; Franz, TJ.* ; Huster, K.M. ; Carayannopoulos, L.N.* ; Yokoyama, W.M.* ; Colonna, M.* ; Siccardi, A.G.* ; Bauer, S.* ; Busch, D.H.

NKG2D-independent suppression of T cell proliferation by H60 and MICA.

Proc. Natl. Acad. Sci. U.S.A. 102, 11805-11810 (2005)
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The activating receptor NKG2D recognizes a wide range of different ligands, some of which are primarily expressed in "stressed" tissues or on tumor cells. Until now, similar stimulatory effects on natural killer and CD8+ T cells have been described for all NKG2D ligands, and the NKG2D receptor/ligand system has therefore been interpreted as a sensor system involved in tumor immune surveillance and activation of immune responses. We show here that the NKG2D ligands H60 and MIC class 1 chain-related protein A (MICA) can also mediate strong suppressive effects on T cell proliferation. Responsiveness to H60- and MICA-mediated suppression requires IL-10 and involves a receptor other than NKG2D. These findings might provide explanations for the observation that strong in vivo NKG2D ligand expression, such as that on tumor cells, sometimes fails to support effective immune responses and links this observation to a distinct subgroup of NKG2D ligands.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter immunology; NKG2D ligands; NKG2D RECEPTOR; CUTTING EDGE; GAMMA-DELTA; NK CELLS; TUMOR-CELLS; IN-VIVO; LIGANDS; ACTIVATION; EXPRESSION; COSTIMULATION
Sprache englisch
Veröffentlichungsjahr 2005
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Quellenangaben Band: 102, Heft: 33, Seiten: 11805-11810 Artikelnummer: , Supplement: ,
Verlag National Academy of Sciences
Begutachtungsstatus Peer reviewed
POF Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Immune Response and Infection
PSP-Element(e) G-520100-001
G-501700-006
PubMed ID 16091471
Erfassungsdatum 2005-12-31