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A phenotypic and functional characterization of NK cells in adenoids
Author(s) -
Mizrahi Sa’ar,
Yefenof Eitan,
Gross Menahem,
Attal Pierre,
Ben Yaakov Avraham,
GoldmanWohl Debra,
Maly Bella,
Stern Noam,
Katz Gil,
Gazit Roi,
Sionov Ronit Vogt,
Mandelboim Ofer,
Chaushu Stella
Publication year - 2007
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0407205
Subject(s) - interleukin 21 , biology , nkg2d , janus kinase 3 , interleukin 12 , lymphokine activated killer cell , nk 92 , cytotoxic t cell , cd49b , microbiology and biotechnology , neural cell adhesion molecule , natural killer cell , immunology , cell , in vitro , cell adhesion , biochemistry , genetics
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 bright CD16 – . 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.