A phenotypic and functional characterization of NK cells in adenoids

被引:10
作者
Mizrahi, Sa'ar
Yefenof, Eitan
Gross, Menahem
Attal, Pierre
Ben Yaakov, Avraham
Goldman-Wohl, Debra
Maly, Bella
Stern, Noam
Katz, Gil
Gazit, Roi
Sionov, Ronit Vogt
Mandelboim, Ofer
Chaushu, Stella [1 ]
机构
[1] Hebrew Univ Jerusalem, Lautenberg Ctr Gen & Tumor Immunol, Hadassah Med Sch, POB 12272, IL-91120 Jerusalem, Israel
[2] Hadassah Sch Dent Med, Jerusalem, Israel
[3] Hadassah Med Ctr, Dept Otolaryngol Head & Neck Surg, IL-91120 Jerusalem, Israel
[4] Hadassah Med Ctr, Dept Obstet & Gynecol, IL-91120 Jerusalem, Israel
[5] Hadassah Med Ctr, Dept Pathol, IL-91120 Jerusalem, Israel
[6] Shaare Zedek Med Ctr, Dept Otolaryngol, Jerusalem, Israel
关键词
human; receptors; chemokines;
D O I
10.1189/jlb.0407205
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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 I (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 CXCL 12 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.
引用
收藏
页码:1095 / 1105
页数:11
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