ADAP is dispensable for NK cell development and function

Lindsey V. Fostel, Joanna Dluzniewska, Yoji Shimizu, Brandon J. Burbach, Erik J. Peterson

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

NK cells are key mediators of the innate immune response and anti-tumor surveillance. Adhesion and degranulation-promoting adapter protein (ADAP, formerly known as SLAP-130 or Fyb) is a hematopoietic-specific adapter that is required for efficient TCR signaling and T cell activation. Herein, we examine a potential role for ADAP in NK development and function. ADAP is expressed in primary NK cells and in IL-2 stimulated lymphokine-activated killers. However, ADAP-deficient mice show no defects in NK development. Further, ADAP is dispensable for key NK functions, including cytotoxicity in response to engagement of activating receptors, cytokine production, conjugate formation and tumor suppression in vivo. These results indicate that, unlike events stimulated by TCR engagement, signaling events engaged by immunoreceptor tyrosine-based activation motif-associated and cytokine receptors on NK cells can occur independently of ADAP.

Original languageEnglish (US)
Pages (from-to)1305-1314
Number of pages10
JournalInternational Immunology
Volume18
Issue number8
DOIs
StatePublished - Aug 2006

Bibliographical note

Funding Information:
We thank Koho Iizuka, Mary Nakamura, Stephen Jameson and Michael Bennett for advice and reagents. Koho Iizuka and Stephen Jameson provided critical review of the manuscript. Grant support was supplied by NIH AI056016-02.

Keywords

  • Adaptor protein
  • Adhesion and degranulation-promoting adapter protein
  • Cytokine secretion
  • Cytotoxicity
  • Inhibitory signaling
  • Ly49 signaling
  • Tumor suppression

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