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 Blood, 26 March 2009, Vol. 113, No. 13, pp. 2955-2964.
Prepublished online as a Blood First Edition Paper on January 5, 2009; DOI 10.1182/blood-2008-06-165944.

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IMMUNOBIOLOGY

Detuning CD8+ T lymphocytes by down-regulation of the activating receptor NKG2D: role of NKG2D ligands released by activated T cells

Cristina Cerboni1, Michele Ardolino1, Angela Santoni1,*, and Alessandra Zingoni1,*

1 Department of Experimental Medicine, Istituto Pasteur-Fondazione Cenci Bolognetti, University of Rome "Sapienza," Rome, Italy

NKG2D is an activating receptor expressed on CD8+{alpha}β+ T cells, {gamma}{delta}+ T cells, natural killer (NK) cells, and some CD4+ T cells. For a long time, the interaction of NKG2D with its ligands (NKG2DLs) MICA, MICB, and ULBP1-3 has been considered a mechanism for recognition and elimination of tumor, infected, or otherwise "stressed" cells. However, a new role for NKG2D as an immunoregulatory receptor is emerging. Here, we show that NKG2D is strongly down-modulated on antigen-activated CD8+ T cells but only if CD4+ T cells are present. Down-modulation was caused by soluble factors produced by CD4+ T cells, and in particular soluble NKG2DLs were found in the supernatants of antigen-activated T-cell cultures. MICB was the ligand released at higher levels when CD4+ T cells were present in the cell cultures, suggesting that it could be the major player of NKG2D down-modulation. CD8+ T cells expressing low levels of NKG2D had impaired effector functions, as evaluated by proliferation, cytokine production, and cytotoxicity assays after combined triggering of NKG2D and TCR-CD3 complex. These findings show that activated CD4+ T cells expressing NKG2DLs can efficiently prevent NKG2D-mediated CD8+ T-cell functions, and suggest that the NKG2D/NKG2DL interaction can regulate immune responses.


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