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Published online before print August 3, 2007

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0407205

Received for publication April 4, 2007.
Revised June 28, 2007.
Accepted for publication June 29, 2007.

Article

A phenotypic and functional characterization of NK cells in adenoids

Sa'ar Mizrahi ^*, Eitan Yefenof ^*, Menahem Gross , David Atal , Avraham Ben Yaakov , Debra Goldman-Wohl , Bella Maly ^||, Noam Stern ^*, Gil Katz ^*, Roi Gazit ^*, Ronit Vogt Sionov ^*, Ofer Mandelboim ^*, and Stella Chaushu ^*¶@

*Lautenberg Center of General and Tumor Immunology, Hebrew University–Hadassah School of Medicine and ^¶Hadassah School of Dental Medicine, founded by the Alpha Omega Fraternity, Jerusalem, Israel; Departments of Otolaryngology–Head and Neck Surgery, Obstetrics and Gynecology, and ^||Pathology, Hadassah Medical Center, Jerusalem, Israel; and Department of Otolaryngology, Shaare Zedek Medical Center, Jerusalem, Israel

^@ To whom correspondence should be addressed. E-mail: drchaushu{at}bezeqint.net.

	Abstract

Adenoids are part of the MALT. In the present study, we analyzed cell surface markers and cytolytic activity of adenoidal NK (A-NK) cells and compared them with NK cells derived from blood of the same donors (B-NK). NK cells comprised 0.67% (0.4–1.2%) of the total lymphoid population isolated from adenoids. The majority (median=92%) of the A-NK cells was CD56^brightCD16^–. A-NK cells were characterized by the increased expression of activation-induced receptors. NKp44 was detected on >60%, CD25 on >40%, and HLA-DR on >50% of freshly isolated A-NK cells. Functional assays indicated that the cytotoxic machinery of A-NK is intact, and sensitive target cells are killed via natural cytotoxicity receptors, such as NKG2D. Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1; CD66) expression was up-regulated in 23% (median) of the A-NK cells by IL-2 activation but unchanged in B-NK cells. CEACAM1 inhibited the A-NK killing of target cells. CXCR4 was expressed on more than 40% A-NK cells prior to activation. Its ligand, CXCL12, was found in endothelial cells of the capillaries within the adenoid and in cells of the epithelial lining. In addition, A-NK cells migrated in vitro toward a gradient of CXCL12 in a dose-responsive manner, suggesting a role for this chemokine in A-NK cell recruitment and trafficking. We conclude that the A-NK cells are unique in that they display an activated-like phenotype and are different from their CD16^– B-NK cell counterparts. This phenotype presumably reflects the chronic interaction of A-NK cells with antigens penetrating the body through the nasal route.

Key Words: human • receptors • chemokines