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

Anja K. Kriegeskorte, Friedemann E. Gebhardt, Simona Porcellini, Matthias Schiemann, Christian Stemberger, Tobias J. Franz, Katharina M. Huster, Leon N. Carayannopoulos, Wayne M. Yokoyama, Marco Colonna, Antonio G. Siccardi, Stefan Bauer, Dirk H. Busch

Research output: Contribution to journalArticlepeer-review

36 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)11805-11810
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume102
Issue number33
DOIs
StatePublished - Aug 16 2005

Keywords

  • Immunology
  • NKG2D ligands

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