2B4 (CD244), NTB-A and CRACC (CS1) stimulate cytotoxicity but no proliferation in human NK cells

The recently described family of SLAM-related receptors plays an important role in the modulation of lymphocyte activity. The members of this family expressed on human NK cells are 2B4 (CD244), NTB-A and CRACC (CS1). The ligands of these surface receptors are also present on all human NK cells, sugg...

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Bibliographic Details
Published in:International immunology 2006-02, Vol.18 (2), p.241-247
Main Authors: Stark, Sebastian, Watzl, Carsten
Format: Article
Language:English
Subjects:
[3H]TdR    [3H]thymidine
Animals
Antibodies, Blocking
Antigens, CD - physiology
Cell Proliferation
cytotoxicity
Cytotoxicity, Immunologic
Glycoproteins - physiology
Humans
Immunoglobulins - physiology
K562 Cells
Killer Cells, Natural - cytology
Killer Cells, Natural - immunology
natural killer cells
proliferation
Receptors, Cell Surface
Receptors, Immunologic - physiology
Signaling Lymphocytic Activation Molecule Family
Signaling Lymphocytic Activation Molecule Family Member 1
SRR    SLAM-related receptor
surface receptors
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Summary:The recently described family of SLAM-related receptors plays an important role in the modulation of lymphocyte activity. The members of this family expressed on human NK cells are 2B4 (CD244), NTB-A and CRACC (CS1). The ligands of these surface receptors are also present on all human NK cells, suggesting that 2B4, NTB-A and CRACC are engaged during the contact of neighboring NK cells. Here we investigate the functional consequence of this interaction. We show that blocking the engagement of 2B4, NTB-A and CRACC has no effect on the proliferation or the development of the cytotoxic potential of human NK cells. However, triggering of 2B4, NTB-A or CRACC by their physiological ligands on MHC class I-negative target cells induces potent NK cell cytotoxicity. This suggests that the engagement of inhibitory receptors by MHC class I on neighboring NK cells blocks 2B4-, NTB-A- and CRACC-induced NK cell cytotoxicity, thereby ensuring that NK cells do not kill each other. In support of this, limiting inhibitory receptor engagement by antibodies leads to the autologous killing of NK cells in a 2B4-, NTB-A- and CRACC-dependent manner.
ISSN:0953-8178
1460-2377
DOI:10.1093/intimm/dxh358