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Cutting Edge: The Adapters EAT-2A and -2B Are Positive Regulators of CD244- and CD84-Dependent NK Cell Functions in the C57BL/6 Mouse

Ninghai Wang, Silvia Calpe, Jill Westcott, Wilson Castro, Chunyan Ma, Pablo Engel, John D. Schatzle and Cox Terhorst
J Immunol November 15, 2010, 185 (10) 5683-5687; DOI: https://doi.org/10.4049/jimmunol.1001974
Ninghai Wang
Division of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115;
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Silvia Calpe
Division of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115;
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Jill Westcott
Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390; and
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Wilson Castro
Division of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115;
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Chunyan Ma
Division of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115;
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Pablo Engel
Department of Cellular Biology and Pathology, Medical School, University of Barcelona, Barcelona, Spain
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John D. Schatzle
Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390; and
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Cox Terhorst
Division of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115;
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Abstract

EWS/FLI1-activated transcript 2 (EAT-2)A and EAT-2B are single SH2-domain proteins, which bind to phosphorylated tyrosines of signaling lymphocyte activation molecule family receptors in murine NK cells. While EAT-2 is a positive regulator in human cells, a negative regulatory role was attributed to the adapter in NK cells derived from EAT-2A–deficient 129Sv mice. To evaluate whether the genetic background or the presence of a selection marker in the mutant mice could influence the regulatory mode of these adapters, we generated EAT-2A–, EAT-2B–, and EAT-2A/B–deficient mice using C57BL/6 embryonic stem cells. We found that NK cells from EAT-2A– and EAT-2A/B–deficient mice were unable to kill tumor cells in a CD244- or CD84-dependent manner. Furthermore, EAT-2A/B positively regulate phosphorylation of Vav-1, which is known to be implicated in NK cell killing. Thus, as in humans, the EAT-2 adapters act as positive regulators of signaling lymphocyte activation molecule family receptor-specific NK cell functions in C57BL/6 mice.

Footnotes

  • The work was supported in part by National Institutes of Health Grants PO1 AI- 065687 (to C.T.) and AI067803 (to J.S.).

  • The online version of this article contains supplemental material.

  • Abbreviations used in this paper:

    B6
    C57BL/6
    EAT-2
    EWS/FLI1-activated transcript 2
    ES cell
    embryonic stem cell
    IP
    immunoprecipitation
    LDH
    lactate dehydrogenase
    SAP
    signaling lymphocyte activation molecule-associated protein
    SLAM
    signaling lymphocyte activation molecule
    wt
    wild-type.

  • Received June 15, 2010.
  • Accepted September 15, 2010.
  • Copyright © 2010 by The American Association of Immunologists, Inc.
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The Journal of Immunology: 185 (10)
The Journal of Immunology
Vol. 185, Issue 10
15 Nov 2010
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Cutting Edge: The Adapters EAT-2A and -2B Are Positive Regulators of CD244- and CD84-Dependent NK Cell Functions in the C57BL/6 Mouse
Ninghai Wang, Silvia Calpe, Jill Westcott, Wilson Castro, Chunyan Ma, Pablo Engel, John D. Schatzle, Cox Terhorst
The Journal of Immunology November 15, 2010, 185 (10) 5683-5687; DOI: 10.4049/jimmunol.1001974

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Cutting Edge: The Adapters EAT-2A and -2B Are Positive Regulators of CD244- and CD84-Dependent NK Cell Functions in the C57BL/6 Mouse
Ninghai Wang, Silvia Calpe, Jill Westcott, Wilson Castro, Chunyan Ma, Pablo Engel, John D. Schatzle, Cox Terhorst
The Journal of Immunology November 15, 2010, 185 (10) 5683-5687; DOI: 10.4049/jimmunol.1001974
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