A phenotypic and functional characterization of NK cells in adenoids.
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.
Lautenberg Center of General and Tumor Immunology, Hebrew University-Hadassah School of Medicine, Jerusalem, Israel.
Sa'ar
S
Mizrahi
Eitan
E
Yefenof
Menahem
M
Gross
Pierre
P
Attal
Avraham
A
Ben Yaakov
Debra
D
Goldman-Wohl
Bella
B
Maly
Noam
N
Stern
Gil
G
Katz
Roi
R
Gazit
Ronit Vogt
RV
Sionov
Ofer
O
Mandelboim
Stella
S
Chaushu
D000234:Adenoids / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D015703:Antigens, CD / Q000378:metabolism; D019002:CD56 Antigen / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002465:Cell Movement; D002470:Cell Survival; D054377:Chemokine CXCL12 / Q000378:metabolism; D002648:Child; D003602:Cytotoxicity, Immunologic; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D058851:GPI-Linked Proteins; D006801:Humans; D007376:Interleukin-2 / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D055655:NK Cell Lectin-Like Receptor Subfamily K; D055629:Natural Cytotoxicity Triggering Receptor 2; D010641:Phenotype; D017452:Receptors, IgG / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism; D055607:Receptors, Natural Killer Cell
D015703:Antigens, CD; D019002:CD56 Antigen; C069847:CD66 antigens; D015815:Cell Adhesion Molecules; D054377:Chemokine CXCL12; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D007376:Interleukin-2; C527085:KLRK1 protein, human; C112837:NCR2 protein, human; D055655:NK Cell Lectin-Like Receptor Subfamily K; D055629:Natural Cytotoxicity Triggering Receptor 2; D017452:Receptors, IgG; D011971:Receptors, Immunologic; D055607:Receptors, Natural Killer Cell