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Departments of
*
Otorhinolaryngology and
Immunology and Parasitology, Yokohama City University, School of Medicine, Yokohama, Japan; and
Tokyo Research Laboratories, Kyowa Hakko Kogyo Co. Ltd., Tokyo, Japan
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The biologic functions of NK cells are modulated by certain cytokines.
IL-2 increases NK cell adhesion on endothelial cells (12). IFN-
and
IL-8 stimulate locomotive ability of NK cells (13, 14). In this study,
we analyzed the effect of IL-12 on NK cell adhesion to endothelial
selectins. IL-12 is a 70-kDa disulfide-linked heterodimeric
glycoprotein composed of 35- and 40-kDa subunits. Some biologic
properties of human IL-12 have been evaluated in vitro. IL-12 is able
to enhance NK/LAK cell cytolytic activity, to augment cytolytic T cell
responses, and to induce secretion of cytokines, particularly IFN-,
from NK cells as well as T cells. Since NK cells have been implicated
as antitumor effector cells and IFN- has been shown to have
antitumor activity in animals, IL-12 has the potential to be used as an
immunomodulatory cytokine in the therapy of malignancies (15, 16).
Furthermore, IL-12 is a chemotactic factor and increases binding
activity of NK cells to endothelium (17). However, the effect of IL-12
on the adhesion of NK cells to selectins has not been analyzed.
To better understand the effect of IL-12 on NK cell adhesion to vascular endothelium and on accumulation of NK cells to inflamed tissue and tumors, we studied the expression of sLex (recognized by KM-93 mAb) and PSGL-1 on IL-12-activated NK cells and analyzed the adhesion activity of activated NK cells to endothelial selectins under flow conditions.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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PL-1 and PL-2 (anti-PSGL-1, mouse IgG1k) were gifts of Dr.
R. P. McEver and Dr. K. L. Moore (University of Oklahoma
Health Sciences Center, Oklahoma City, OK). KM-93 (mouse IgM) against
sLex was purchased from Seikagaku-Kogyo (Osaka, Japan).
H18/7 (anti-E-selectin, IgG2a) mAb and GA6 (anti-P-selectin,
IgG1k) mAb were purchased from Becton Dickinson (San Jose, CA). UCHT-1
(anti-CD3, IgG1) mAb, M5E2 (anti-CD14, IgG2a), HIB19
(anti-CD19, IgG1) mAb, DREG-56 (anti-CD62L, IgG1
) mAb, C8.6
(anti-human IL-12, IgG1) mAb, phycoerythrin-conjugated
anti-CD16 (3G8, IgG1) mAb, isotype-matched control mouse IgG1,
IgG2a, and IgM were purchased from PharMingen (San Diego, CA).
FITC-labeled rabbit anti-mouse Ig and FITC-labeled anti-human
IgG were purchased from Dako (Glostrup, Denmark). Control human IgG was
purchased from Sigma Japan (Tokyo, Japan). Rat anti-mouse IgG1 MACS
beads were purchased from Miltenyi Biotec (Auburn, CA).
Chemicals, reagents, and cytokines
Human IL-2 was a gift from Takeda Pharmaceutical (Osaka, Japan). Recombinant human IL-12 was purchased from R&D Systems (Minneapolis, MN).
Fractionation of cells
Mononuclear cells were isolated from heparinized peripheral blood collected by venipuncture from healthy donors. The blood was diluted with an equal volume of 0.9% NaCl and layered over Ficoll/Hypaque-Lymphoprep (Nycomed, Oslo, Norway). Mononuclear cells were enriched through depletion of cells that adhered to plastic by incubation at 37°C for 2 h, and plastic-nonadherent cells were harvested. To isolate NK cells, this population was incubated with anti-human CD3 and CD19 mAbs for 30 min at 4°C. The cells were washed twice in PBS with 1% BSA and further incubated with goat anti-mouse IgG-conjugated magnetic beads for 30 min at 4°C. The cells were then washed twice and applied to the column in a magnetic cell separator to deplete T cells and B cells. The negative fraction was harvested. Flow cytometric analysis revealed the resulting NK cell population contained CD16+ > 95%, 2% > CD3+, 2% > CD19+, and 2% > CD14+. Neutrophils were isolated from heparinized blood using Monopoly resolving medium (Dainippon Pharmaceutical, Osaka, Japan). Neutrophils were 85% pure as assessed by Wright-Giemsa staining.
In cell culture studies, NK cells (106 cells/ml) were cultured in AIM V medium (Life Technologies, Gaithersburg, MD). NK cells were activated with 0.5 ng/ml IL-12 in the culture medium for 96 h.
Cell lines
Chinese hamster ovary (CHO) cells expressing a stably
transfected human P-selectin cDNA (CHO P-selectin) were obtained from
Dr. G. R. Larsen (Genetics Institute, Cambridge, MA). E-selectin
molecules expressing CHO cells were constructed as described previously
(18). Transfected CHO cells were cultured in MEM
(Life Technologies)
containing 10% FCS, antibiotics, L-glutamine, and
essential amino acids.
FACS analysis of NK
For indirect immunofluorescence, resting NK cells and IL-12-activated NK cells were incubated with KM-93 or PL-1 for 30 min at 4°C. After being washed with PBS, cells were stained with FITC-conjugated anti-mouse Ig. Furthermore, the resting NK cells and IL-12-activated NK cells were preincubated on ice for 30 min with 10% human serum in PBS to block Fc receptor and washed three times with 10% human serum in PBS. These cells (106 cells) were incubated with P-selectin-IgG chimera (50 µl, 20 µg/ml) and 2 mM Ca2+, after preincubation with anti-human IgG-FITC (final concentration, 5.6 µg/ml) on ice for 1 h for conjugation of P-selectin-IgG with FITC. A P-selectin-IgG chimera was produced as described previously (19). In some experiments, NK cells were pretreated with anti-PSGL-1 mAb (10 µg/ml, for 30 min on ice) before incubation with P-selectin-IgG. In others, the cells were incubated with P-selectin-IgG in presence of anti-P-selectin mAb. For negative control staining, we used human IgG preincubated with anti-human IgG-FITC. Expression was analyzed on a Becton Dickinson FACScan with CellQuest analysis software.
Attachment of NK cells to E-selectin and P-selectin under flow conditions
Transfected CHO cells were cultured in capillary tubes. The model of flow conditions was described previously (19). A tube was attached to the end of a glass capillary tube, and the glass capillary tube was connected to a syringe pump (TERUMO, Tokyo, Japan) fitted with a 50-ml syringe to establish laminar flow. The wall shear stress was calculated by Poiseuille’s law of Newtonian fluids, with viscosity of 0.01 P (at room temperature). The wall shear stress in dynes/cm2 = [(mean flow velocity x 8)/(tube diameter x viscosity)]. The tube was mounted on an Olympus (Tokyo, Japan) inverted microscope. Interaction of NK cells with selectin-transfected CHO cells was observed and videotaped for 10 min.
In the flow system, 1 x 106 NK cells/ml of binding medium with 2 mM Ca2+ were caused to flow across transfected CHO cells in the capillary tubes using a syringe pump. The adhesion of NK cells to selectins expressed on transfected CHO cells was determined at variable rates of shear stress. The numbers of adherent cells was examined by counting four to six fields (x200) under an inverted microscope during the entire 10-min experiment.
Rolling velocities of at least 10 cells under each microscope field were measured. At a given shear stress, we observed four to six microscopic fields. Photographs were taken as real time images to mark the location of NK cells. The displacement of the center of individual cells was measured 10 s later.
For Ab inhibition assays, E-selectin-transfected CHO cells in the capillary tubes were first treated with anti-E-selectin mAb or isotype control mouse IgG2a (20 µg/ml for 30 min). P-selectin-transfected CHO cells were treated with anti-P-selectin mAb or isotype-matched control. Furthermore, NK cells were treated with anti-sLex mAb (KM-93, 50 µg/ml for 30 min), anti-CD62L (DREG-56, 20 µg/ml for 30 min), or anti-PSGL-1 mAb (PL-1 and PL-2, 10 µg/ml for 30 min) in some experiments.
The data shown in this study are the results of a representative experiment among more than three independent experiments. The error bar represents the SD. The results are expressed as means ± SD/field.
Statistical analysis
Data were compared through analysis of variance using the unpaired Student’s t test, and p < 0.05 was considered to represent a significant difference between group means.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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We analyzed the expression of PSGL-1 on resting and
IL-12-activated NK cells and the binding of soluble P-selectin-IgG to
resting and IL-12-activated NK cells. IL-12-activated NK cells
contained CD16+ > 95%, 3% > CD3+. Most
resting and IL-12-activated NK cells expressed PSGL-1 recognized by
PL-1 mAb (Fig. 1
, A and
B). The mean channel fluorescence value for PSGL-1 on
resting NK cells was 143 ± 26, and that on activated NK cells was
161 ± 30. The percentage of resting NK cells bound to soluble
P-selectin-IgG was 
15% (Fig. 1C). Binding of soluble
P-selectin-IgG to NK cells was completely abolished in the presence of
anti-P-selectin mAb (Fig. 1E). The percentage of
IL-12-activated NK cells bound to soluble P-selectin-IgG was about 65%
(Fig. 1D). Addition of anti-P-selectin mAb decreased the
binding of soluble P-selectin-IgG to activated NK cells (Fig. 1F). When NK cells were cultured with IL-12 in the presence
of anti-IL-12 mAb (C8.6, 10 µg/ml), binding of soluble
P-selectin-IgG was similar to that of resting NK cells (data not
shown). Neutrophils, as a positive control, bound efficiently to
soluble P-selectin-IgG (Fig. 1G). Binding of soluble
P-selectin-IgG to neutrophils was inhibited in the presence of
anti-P-selectin mAb.
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We analyzed the expression of sLex on resting and
IL-12-activated NK cells. For detection of sLex on NK
cells, we used KM-93 mAb. KM-93 was reactive with resting and activated
NK cells (Fig. 2). The mean channel
fluorescence value for sLex on resting NK cells was
110 ± 28. On the other hand, the mean fluorescence value for
sLex on IL-12-activated NK cells was 520 ± 130. The
expression of sLex on NK cells incubated with IL-12 in the
presence of anti-IL-12 mAb (C8.6 10 µg/ml) was similar to that of
resting NK cells (data not shown). Thus, the expression of
sLex on NK cells increased significantly by IL-12
activation.
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We examined the adhesion activity of resting and IL-12-activated
NK cells to P-selectin transfectant under flow conditions. Resting and
activated NK cells tethered and rolled on P-selectin transfectant under
shear stress between 0.8 and 2.5 dynes/cm2. At 3.0
dynes/cm2, the binding of NK cells to P-selectin
transfectant was not significant (Fig. 3A). The number of activated
NK cells bound to P-selectin transfectant was higher than that of
resting NK cells under shear stress below 1.5 dynes/cm2.
Above 2.0 dynes/cm2, the difference between the number of
adherent resting NK cells and adherent activated NK cells decreased.
The interactions of resting and activated NK cells with P-selectin
transfectant were completely abolished by pretreatment of P-selectin
transfectant with anti-P-selectin mAb.
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B). Effect of treatment with anti-L-selectin, anti-sLex, or anti-PSGL-1 (PL-1 or PL-2) mAbs on NK cell adhesion to P-selectin transfectant under flow conditions
We examined the P-selectin ligands of NK cells. Resting (Fig. 4A) and IL-12-activated NK
cells (Fig. 4B) were preincubated with anti-L-selectin,
anti-sLex, anti-PSGL-1 (PL-1 or PL-2), or control
mAbs. The treated resting and activated NK cells were perfused across
the P-selectin transfectant monolayers under shear stress at 1.5
dynes/cm2. Treatment of resting and activated NK cells with
anti-PSGL-1 (PL-1) mAb reduced the level of NK cell adhesion to
P-selectin transfectant. Treatment of resting and activated NK cells
with anti-L-selectin, anti-sLex, or anti-PSGL-1
(PL-2) mAbs did not reduce the level of NK cell adhesion. Treatment
with control isotype-matched mAb (IgG1) had no inhibitory effect
(data not shown). The PL-1 epitope is within or distal to a
serine/threonine-rich region of the PSGL-1 polypeptide that is cleaved
by O-sialoglycoprotein endopeptidase, whereas the PL-2
epitope is more proximal to the membrane (11). PL-1, but not PL-2
inhibited the binding of NK cells to P-selectin. These findings
indicated that PSGL-1 was the major ligand of NK cells for P-selectin,
and the O-linked glycans on PSGL-1 on NK cells played an
important role in P-selectin/PSGL-1 interaction.
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We examined the adhesion activity of resting and IL-12-activated
NK cells to E-selectin under flow conditions. Resting and activated NK
cells tethered and rolled on E-selectin transfectant under shear stress
between 0.8 and 2.5 dynes/cm2. At 3.0
dynes/cm2, the binding of NK cells to E-selectin
transfectant was not significant (Fig. 5A). The number of activated
NK cells bound to E-selectin transfectant was higher than that of
resting NK cells under shear stress below 1.5 dynes/cm2.
Above 2.0 dynes/cm2, the differences between the number of
adherent resting NK cells and adherent activated NK cells decreased.
The interactions of resting and activated NK cells with E-selectin
transfectant were completely abolished by pretreatment of E-selectin
transfectant with anti-E-selectin mAb.
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B). Effect of treatment with anti-L-selectin, anti-PSGL-1, or anti-sLex mAbs on NK cell adhesion to E-selectin transfectant under flow conditions
We examined the E-selectin ligands of NK cells. Resting (Fig. 6A) and IL-12-activated (Fig. 6B) NK cells were preincubated with anti-L-selectin,
anti-PSGL-1, anti-sLex, or control mAbs. The
treated resting and activated NK cells were perfused across the
E-selectin transfectant monolayers under shear stress at 1.5
dynes/cm2. Treatment of resting and activated NK cells with
anti-sLex mAb reduced the level of NK cell adhesion to
E-selectin transfectant. Treatment of resting NK cells with
anti-L-selectin mAb slightly reduced the level of adhesion, but the
reduction was not significant. In contrast, treatment of resting NK
cells with anti-PSGL-1 mAb and of activated NK cells with
anti-L-selectin or anti-PSGL-1 mAb did not block adhesion.
Treatment with control isotype-matched mAb (IgG1 and IgM) was not
inhibitory (data not shown). These findings indicated that
sLex was the major ligand of NK cells for E-selectin.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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C and 4A). PSGL-1 is expressed
on most lymphocytic cells, while soluble P-selectin binding is evident
in only some lymphocytic populations (21). During in vitro stimulation,
the percentage of peripheral blood T lymphocytes bound to P-selectin
increased. In our study, IL-12 activation increased the percentage of
NK cells bound to soluble P-selectin-IgG from 15% to 65% (Fig. 1, C and D). Therefore, NK cells increased the
expression of the P-selectin ligands by IL-12 activation. During
activation, the difference between the mean fluorescence value for
PSGL-1 on resting and activated NK cells was not high (Fig. 1, A and B). Other populations of lymphocytes are
similar to NK cells. Most CD4+ T cells express PSGL-1.
Although memory T cells or Th1 can bind to P-selectin, naive or Th2
cannot bind to P-selectin (22-24). In contrast, soluble-phase
P-selectin can bind to PSGL-1 on almost all neutrophils and monocytes
(11). Neutrophils and monocytes were reported to express the high
affinity form of PSGL-1 for P-selectin (11). In our studies, the
treatment of resting and activated NK cells with
anti-sLex mAb did not reduce the level of adhesion to
P-selectin (Fig. 4). In contrast, sLex structure of PSGL-1
molecule plays a role in neutrophil and HL-60 adhesion to P-selectin
(20, 25). Fuhlbrigge et al. (26) have reported recently that cutaneous
lymphocyte Ag (CLA)-positive and CLA-negative T cell populations
tethered and rolled on P-selectin with comparable efficiency and that
neither CLA nor sLex is required for P-selectin ligand
activity on T cells. Alone et al. (27) reported that HECA-452
reactivity on different T clones did not correlate with the level of
P-selectin binding activity. Thus, PSGL-1 expressed on NK cells may
contain carbohydrate ligands other than the sLex structure
for binding to P-selectin, and NK cells may require alteration of
PSGL-1 glycosylation, induced by cytokine activation, for up-regulation
of its adhesive function.
NK cells can roll on E-selectin via the sLex recognized by
KM-93 mAb (Fig. 5A). Pinola et al. (9) reported that NK
cells adhered to E-selectin and expressed the sialylated
Lex structure. This sLex epitope on NK cell was
weakly reactive with the CSLEX-1 mAb (9, 28) but was identified
strongly by KM-93 and FH-6 mAbs (Fig. 2A) (8). Pinola
et al. reported that treatment with KM-93 mAb partially inhibited NK
cell adhesion to E-selectin but that HL-60 adhesion to E-selectin was
completely inhibited by treatment with KM-93 mAb. In our study, under
flow conditions, treatment of resting NK cells with KM-93 mAb resulted
in 70% reduction of NK cell binding to E-selectin (Fig. 6A). However, the omission of the number of adherent
resting NK cells to E-selectin by treatment with anti-L-selectin
mAb was not clear.
IL-12 activation of NK cells increased the expression of
sLex and the level of adhesion to E-selectin under flow
conditions (Figs. 2 and 5A). Leung et al. (29) reported that
IL-12 could increase expression of CLA on T cells activated with Ag or
superantigen and thereby increase their efficiency of recirculation to
the skin, including areas with vascular E-selectin. Furthermore,
CD4+ T cells incubated in the presence of IL-12 and IFN-
for the generation of Th1 could bind to E-selectin more effectively
than those stimulated by IL-2 and IL-4 for the generation of Th2 (23, 24). Thus, IL-12 could increase the E-selectin ligands on T and NK
cells and thereby promote their binding to E-selectin. Furthermore,
Sasaki et al. (30) reported that fucosyltransferase VII transfected
Namalwa KJM cells could bind to E-selectin and that this binding was
blocked by anti-sLex mAb (KM-93). Wagers et al. have
reported that transfection of fucosyltransferase VII cDNA could confer
E-selectin binding ability with K-562 (31). IL-12 stimulation may
increase the level of fucosyltransferase VII of NK cells.
NK cells are cytotoxic without prior sensitization for a wide range of
target cells, including some microorganisms and virus-infected and
transformed cells. and have a central role in the regulation of immune
response and hemopoiesis. The cytotoxic activity and cytokine
production of NK cells is regulated by IL-12. In recruitment,
extravasation, and accumulation of leukocytes at certain pathologic
sites, carbohydrate ligand/endothelial selectin interactions play an
important role. Our study demonstrates that IL-12 increased the
expression of sLex, E-selectin ligand, augmented the
binding of PSGL-1 for P-selectin, and thereby increased the adhesion
activity of NK cells to endothelial selectins under flow conditions.
The IL-12 activation of NK cell adhesion is suggested to be important
for migration and accumulation of NK cells into infection sites or
tumor sites. At local infection sites, macrophages, Langerhans cells,
or other cell types produce IL-1 and TNF-. Local production of IL-1
and TNF- can induce the expression of E-selectin on endothelium, and
TNF- can induce the expression of P-selectin on endothelium (32, 33). Furthermore, Melder et al. (5) reported that tumor interstitial
fluid increased the expression of E-selectin and VCAM-1 on endothelium.
Fox et al. (6) reported that the expression of E-, P-selectin, and
ICAM-3 increased on breast cancer endothelium in contrast to normal
breast endothelium. Under these pathologic conditions, it is suggested
that IL-12 effectively enhances the infiltration of NK cells at target
sites.
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Acknowledgments |
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Mutsuhiko Minami, Department of Immunology and Parasitology, Yokohama City University, School of Medicine, Fukuura 3-9, Kanazawa-ku, Yokohama 236, Japan.
3 Abbreviations used in this paper: sLex, sialyl-Lewisx; PSGL-1, P-selectin glycoprotein ligand-1; CHO, Chinese hamster ovary; CLA, cutaneous lymphocyte antigen.
Received for publication November 26, 1997. Accepted for publication March 27, 1998.
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References |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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1,3-fucosyltransferase that is involved in biosynthesis of the sialyl Lewis X carbohydrate determinants in leukocyte. J. Biol. Chem. 269:14730.1,3 fucosyltransferase, FucT-VII, in leukocyte adhesion to E-selectin. Blood 88:2125. activated endothelium under flow. J. Exp. Med. 181:1179.-activated vascular endothelium under flow in vitro. J. Immunol. 156:326.
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, The number of resting NK
cells bound to control CHO cells; 
, The number of IL-12-activated NK
cells bound to control CHO cells. * p < 0.05.
B, Comparison of the rolling velocities of resting and
activated NK cells on P-selectin transfectant under shear stress at
1.0, 1.5, and 2.0 dynes/cm2. Their rolling velocities at
each shear stress were calculated as described in Materials and
Methods.
