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Blood, 1 January 2005, Vol. 105, No. 1, pp. 233-240.
Prepublished online as a Blood First Edition Paper on August 24, 2004; DOI 10.1182/blood-2004-03-1075.
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IMMUNOBIOLOGY
NKG2D receptor–mediated NK cell function is regulated by inhibitory Ly49 receptors
Jeyarani Regunathan,
Yuhong Chen,
Demin Wang, and
Subramaniam Malarkannan
From the Blood Research Institute, Blood Center of Southeastern Wisconsin, Milwaukee; Department of Microbiology/Molecular Genetics, Medical College of Wisconsin, Milwaukee; and Department of Medicine, Medical College of Wisconsin, Milwaukee.
Interaction of the activating ligand H60 with NKG2D receptor constitutes a major stimulatory pathway for natural killer (NK) cells. The influence of inhibitory Ly49 receptors on NKG2D-mediated activation is not clearly understood. Here we show that the magnitude of NKG2D-mediated cytotoxicity is directly proportional to both the levels of H60 and the nature of major histocompatibility complex (MHC) class I molecules expressed on the target cells. The expression levels of H60 on the target cells determined the extent to which the inhibition by Ly49C/I receptors can be overridden. In contrast, even a higher expression of H60 molecule on the target cells failed to overcome the inhibition mediated by Ly49A/G receptors. Also, the level of interferon- (IFN-) and granulocyte-macrophage colony-stimulating factor (GM-CSF) generated by NK cells through anti-NKG2D monoclonal antibody (mAb)-mediated activation is significantly reduced by the presence of immobilized anti-Ly49A/G mAbs. Thus, NKG2D-mediated cytotoxicity and cytokine secretion results from the fine balance between activating and inhibitory receptors, thereby defining the NK cell-mediated immune responses. (Blood. 2005;105:233-240)
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