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Joint Program in Transfusion Medicine, Children’s Hospital, Boston, MA 02115;
Department of Pathology, Harvard Medical School, Boston, MA 02115;
Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305;
Center for Molecular Biology and Medicine, Veterans Affairs, Palo Alto Health Care System, Palo Alto, CA 94304;
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Millennium Pharmaceuticals, Cambridge, MA 02142; and
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Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResults and DiscussionReferences |
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. CD16- NK cells were the only
CD56+ population that uniformly expressed trafficking
molecules necessary for homing into secondary lymphoid organs through
high endothelial venule. These findings describe a diverse population
of cells that may have trafficking patterns entirely different from
each other, and from other lymphocyte types. |
Introduction |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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The other major division of the CD56+ population is composed of cells from the T lineage. These CD3+/CD56+ cells are known as cytokine-induced killer (4, 5), or NK-T cells (due to their functional similarities to murine CD3+/NK1.1+ NK-T cells). The human PBL NK-T population is enriched in CD8 T cells of effector phenotype (6). Like murine NK-T cells (7), human NK-T cells contain a subset that can recognize lipid Ags presented by the HLA/MHC class I-like molecule CD1d (8).
Chemokines are a large family of small proteins involved in leukocyte trafficking (9, 10, 11, 12). Heterogeneity of chemokine receptor expression by PBL subsets has recently been shown to contribute to tissue-specific homing of T cell subsets (13, 14, 15, 16) (reviewed in Refs. 13 and 14).
In contrast, little is known about the homing properties of the CD56+ PBL subsets. Surveys of expression patterns for individual chemokine receptors on PBLs have demonstrated the presence of several such receptors on CD56+ cells. For example, CD56+ cells have been variously reported to express CXC chemokine receptor (CXCR)3 1 (15), CCR2 and CCR5 (16), CCR7 (17), and CX3CR1 (18). However, little attempt has been made to carefully ascertain the differences in chemokine receptor expression patterns among the various CD56+ subsets. In addition, many published studies have relied on in vitro activated cells (19, 20). Since the vast majority of circulating lymphocytes are not activated, we feel strongly that the repertoire of receptors expressed by fresh, resting cells is most relevant toward elucidating which receptors may be directly involved in vivo with egress from the blood.
CD56+ lymphocytes are believed to be major players in immunosurveillance and antitumor responses (1, 21, 22). Thus, the mechanisms by which these cells home into tumors and areas of inflammation are of great relevance to human health and disease. To shed light on the homing potentials of CD56+ subsets, we have undertaken to systematically examine the chemokine receptor repertoires of the three PBL types mentioned above: CD16+ NK, CD16- NK, and NK-T. We have studied the differential enrichment of each subset after migration to individual chemokines, as well as the expression of known chemokine receptors by each subset and the relationship between receptor expression and the ability to migrate toward known ligands.
We have found dramatic differences between the chemokine receptor repertoires of NK vs NK-T cells, as well as between CD16+ and CD16- NK cells. These differences imply that NK and NK-T cells may have entirely different routes of circulation and trafficking patterns. We have also found that, although CD16+ and CD16- NK cells are each relatively uniform in their expression of receptors, NK-T cells are extremely heterogeneous. This implies that the NK-T population may itself be further divided into previously unrecognized subpopulations.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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The following unconjugated mouse anti-human mAbs were used in this study: CCR1, 2D4 (IgG1; Millennium Pharmaceuticals, Cambridge, MA) and 53504 (IgG2b; R&D Systems, Minneapolis, MN); CCR2, 48607 (IgG2b; R&D Systems); CCR3 (IgG2a; Millennium Pharmaceuticals); CCR4, 1G1 (IgG1; Millennium Pharmaceuticals) and 2B10 (IgG2a; Millennium); CCR5, 2D7 (IgG2a; BD PharMingen, San Diego, CA); CCR6, 53103 (IgG2b; R&D Systems); CCR7, 7H12 (IgG2b; Millennium Pharmaceuticals) and 3D9 (IgM; Millennium Pharmaceuticals); CCR9, 96-1 (IgG1; Millennium Pharmaceuticals) and 3C3 (IgG2b; Millennium Pharmaceuticals); CXCR1, 5A12 (IgG2b; Millennium Pharmaceuticals); CXCR2, 6C6 (IgG1; BD PharMingen) and 48311 (IgG2a; R&D Systems); CXCR3, 1C6 (IgG1; Millennium Pharmaceuticals) and 49801 (R&D Systems); CXCR4, 12G5 (IgG2a; BD PharMingen) and 44716 (IgG2b; R&D Systems); CXCR5, 51505 (IgG2b; R&D Systems); CX3CR1, 1E5 (IgG1; Millennium Pharmaceuticals); Bonzo, 56811 (IgG2b; R&D Systems); L-selectin, DREG-56 (IgG1; Butcher laboratory staff) and DREG-200 (IgG1; Butcher laboratory staff). Unconjugated mAbs were visualized with biotinylated horse anti-mouse IgG (Vector Laboratories, Burlingame, CA), followed by streptavidin PerCP (Becton Dickinson, San Jose, CA). In all cases in which more that one mAb was used for a given receptor, both mAbs behaved comparably.
Directly conjugated mAbs
The following directly conjugated mouse anti-human mAbs were obtained from BD PharMingen: CD16 FITC (3G8); CD56 PE (B-159); and CD3 APC (UCHT-1).
Chemokines
The following human chemokines were used in this study:
stromal-derived factor (SDF)-1
, synthetic (from Gryphon Sciences,
South San Francisco, CA) and recombinant (PeproTech, Rocky Hill, NJ);
macrophage-inflammatory protein (MIP)-3, synthetic (made by the
author D.S.) and recombinant (PeproTech); secondary lymphoid tissue
chemokine (SLC), recombinant (R&D Systems); IFN-
-inducible T cell
chemoattractant (ITAC), synthetic (made by the author D.S.);
IFN--induced protein-10 (IP-10), recombinant (PeproTech);
MIP-3, synthetic (Gryphon); RANTES, recombinant (PeproTech);
MIP-1, recombinant (PeproTech); monocyte chemoattractant protein
(MCP)-3, recombinant (PeproTech); MCP-1, recombinant (PeproTech); IL-8,
recombinant (PeproTech); soluble fractalkine, synthetic (Gryphon) and
recombinant (R&D Systems); monocyte-derived chemokine, synthetic
(made by the author D.S.); thymus-expressed chemokine, recombinant
(PeproTech). In all cases in which more than one chemokine was tested,
each responded comparably with the other.
There are a large number of overlapping ligand/receptor systems (at
least 12) for CCR1, CCR2, CCR3, and CCR5. The chemokines that bind one
or more of these receptors include MIP-1, MIP-1, RANTES,
MCP-1–4, Eotaxin-1–3, and hemofiltrate C-C chemokine-1, 2, and
4 (12). Thus, instead of testing each of these chemokines
on the CD56 subsets (which would be extremely redundant), we included
the four chemokines in the panel such that each of the above receptors
is bound by two chemokines: CCR1, by RANTES and MCP-3; CCR2, by MCP-1
and MCP-3; CCR3, by RANTES and MCP-3; CCR5, by MIP-1 and RANTES.
Migration assays
Preparation of human lymphocytes, migration through 5-µm transwells, calculation of migration in percentage input, and calculation of percentage of specifically migrated cells were all performed as previously described (23, 24).
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Results and Discussion |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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). NK-T cells are distinguished from NK
cells by CD3 expression, and comprise 
5% of total PBLs in normal
healthy adult donors. These cells express TCR rather than
TCR
; variably express CD8 and CD8; and only very rarely
express CD4 (data not shown). The CD3- NK cells
can be further divided into CD16+ and
CD16- subsets (Fig. 1). The
CD16+ NK cells comprise 5% of PBLs. The
CD16- NK cells comprise 1% of PBLs, and
express higher levels of CD94 (data not shown) and CD56 than
CD16+ NK cells, as described elsewhere
(3). In fact, the small CD56high
population separated from the bulk of the CD56+
cells visible in the histogram (Fig. 1, left panel) is
composed entirely of this latter population.
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Little is known about the tissue tropisms or homing
receptor/chemokine receptor profiles of CD56+
lymphocyte subsets. In an attempt to shed light on this issue, we
designed a process to screen several chemokines on each cell type,
using migration assays (Fig. 2). After
compensation for spontaneously migrated cells, the process allowed us
to detect enrichment (or depletion) of a given lymphocyte subtype (this
method was successfully used in a previous study to detect enrichment
of skin-homing cells after migration of lymphocytes to CCR4 ligands
(24)).
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), and the migrated populations were immunophenotyped for
comparison with the starting population.
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). SDF-1 was the only case in which
each population studied was neither enriched nor depleted (with respect
to the starting population) after migration to the chemokine. This is
consistent with the notion that SDF-1 attracts essentially all PBLs
with equal efficiency (23, 25). The role of such a
universally expressed chemokine receptor in lymphocyte trafficking
remains unclear.
CD16+ NK cells.
CD16+ NK cells comprised >50% of the
populations migrated to IL-8 and to soluble fractalkine, 10-fold
enrichments over their representation in the starting population (Fig. 2, upper left panel). Migrated populations for all other
tested chemokines contained depleted numbers of
CD16+ NK cells, with the exception of SDF-1
(as mentioned above).
NK-T cells.
In contrast to the findings for CD16+ NK cells,
NK-T cells were only slightly enriched in the soluble
fractalkine-migrated population, and were slightly depleted in the
IL-8-migrated population (Fig. 2, lower left panel). Like
CD16+ NK cells, NK-T cell representation was
maintained in the SDF-1-migrated population. NK-T cells were
dramatically enriched in the MIP-1-migrated population, comprising
nearly 75% in contrast to 5% of the starting population, a
15-fold increase. NK-T cells were also somewhat enriched in the
populations attracted to MIP-3, MCP-1, MCP-3, RANTES, ITAC, and
IP-10.
CD16- NK cells.
CD16- NK cells behaved much more like NK-T cells
than like CD16+ NK cells (Fig. 2, lower
left panel). Although these cells comprised only <1% of the
starting population, they represented 10% of the population
attracted to MIP-1 (Fig. 2, lower left panel). Like NK-T
cells, the CD16- NKs were moderately enriched by
MCP-3, RANTES, ITAC, and IP-10. Unlike the other two CD56 subsets
studied, the CD16- NK cells were not depleted in
the populations migrated to the CCR7 ligands MIP-3 and SLC.
For comparison, naive CD4 T cells from the same donors were also tested
in this assay, in parallel with the CD56+ subsets
(Fig. 2, upper right). As previously described
(24), naive CD4 T cell numbers were maintained (or
slightly enriched) only in the populations attracted to SDF-1,
MIP-3, and SLC.
Expression of receptors by CD56+ lymphocyte subsets
In keeping with the migration patterns seen in Fig. 2, NK
and NK-T cells differed greatly in their cell surface receptor
expression.
CD16+ NK cells.
CD16+ NK cells uniformly expressed CXCR1 and
CX3CR1 at high levels, consistent with the predominance of this
population in the IL-8- and soluble fractalkine-attracted populations
(Fig. 3, top rows). CXCR4, the
receptor for SDF-1, was also present at high levels on these cells.
CXCR2 and CXCR3 were present at lower levels. Chemokine receptors
CCR1–7 and CCR9 were absent on this population, as well as CXCR5 and
the orphan chemokine receptor Bonzo. Expression of the lymph node
homing receptor L-selectin was variable.
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, bottom rows). CCR5, CCR7, CXCR3, and CXCR4 were uniformly
expressed at high levels on this population. CCR1–4, 6, and 9 were not
expressed, nor were CXCR2 and CXCR5. L-selectin was highly expressed on
this population.
NK-T cells.
In contrast to the uniform expression patterns observed among the NK
populations, NK-T cells often expressed chemokine receptors in a
heterogeneous or bimodal fashion (Fig. 3, middle rows). Like
CD16- NK cells, NK-T cells expressed uniformly
high levels of CCR5, CXCR3, and CXCR4. However, CCR1, CCR2, CCR6,
CX3CR1, and Bonzo were heterogeneously expressed. CXCR1 expression was
variable among donors, but was generally absent. Only CCR3, 4, 7, 9,
and CXCR2 were consistently absent from this population.
Direct comparison of chemotactic responses among CD56+ lymphocyte subsets
To comprehensively determine whether chemokine receptor expression
(as detected by flow cytometry) correlates with responsiveness to
chemokines, known ligands for each receptor were titered on the three
CD56+ subsets in migration assays. As expected,
all three CD56+ subsets responded equally well to
SDF-1, and with very similar dose-response curves (Fig. 4, upper left panel).
CD16+ NK cells.
Both IL-8 and soluble fractalkine strongly attracted
CD16+ NK cells, but had much smaller effects on
CD16- NK cells and NK-T cells (Fig. 4, filled
squares). This correlates well with the high expression of CXCR1 and
CX3CR1 on CD16+ NK cells, but not on the other
two subsets. CD16+ NK cells responded moderately
to the CXCR3 ligands ITAC and IP-10, in keeping with their expression
of CXCR3. NK cells also responded moderately to high doses of MIP-3,
although CCR6 (the only known receptor for MIP-3) was not
detected by FACS. No appreciable migration was detected to any of the
other chemokines tested.
NK-T cells.
MIP-1 attracted NK-T cells much better than it attracted either type
of NK cell (Fig. 4, gray triangles). However, despite the fact that
NK-T cells were greatly enriched by migration to MIP-1 (Fig. 2), and
expressed very high levels CCR5 (the only known receptor for CCR5 in
humans; Fig. 3), MIP-1 was only a poor attractor. A reasonable
explanation for this apparent discrepancy may be that MIP-1 performs
poorly in the transwell assay system: it may have a shorter
t1/2 in migration medium or may adhere
to plastic more that other chemokines. Thus, although the amplitude of
migration to MIP-1 is poor for PBLs, this would explain why the
differential effects of MIP-1 on NK-T cells vs all other PBL subsets
can still be detected in the enrichment assay (Fig. 2). NK-T cells
responded well to RANTES, another CCR5 ligand (Fig. 4, gray triangles).
However, RANTES also interacts with CCR1, so its effects may not be
entirely through CCR5. NK-T cells responded moderately to MIP-3 and
SLC, although CCR7 was observable only on small numbers of NK-T cells
by flow cytometry. NK-T cells responded well to MCP-2, MIP-3, ITAC,
and IP-10, in keeping with CCR2, CCR6, and CXCR3 expression on NK-T
subpopulations (Fig. 4, gray triangles).
CD16- NK cells.
CD16- NK cells responded most dramatically to
the CCR7 ligands MIP-3 and SLC, and to the CXCR3 ligands ITAC and
IP-10 (Fig. 2, open circles). Chemotactic responses of
CD16- NK cells to other ligands were largely
parallel to those of NK-T cells, with the exception of MCP-1. Unlike
NK-T cells, CD16- NK cells responded poorly to
MCP-1 (Fig. 4, open circles), and did not express CCR2, the only known
receptor for MCP-1 (Fig. 3). CD16- NK cells
showed little or no response to IL-8 or soluble fractalkine, which were
the predominant attractants of CD16+ NK
cells.
Chemokine receptors provide clues to differential homing of CD56+ subsets
This comprehensive analysis of the various
CD56+ lymphocyte subsets from human peripheral
blood has demonstrated a great diversity of receptor expression, and
therefore of homing potential. Recently, expression of particular
chemokine receptors was found to be associated with subsets of
peripheral blood CD4 T cells known to home preferentially through
particular tissue types. CCR4 is expressed at high levels on
CLA+ memory CD4 cells, which are known to home
preferentially through cutaneous sites (24). CCR9 is
expressed only on a subset of
47
integrin-expressing memory CD4 cells, which home preferentially through
mucosal tissues (26). Neither CCR4 nor CCR9 was observed
on CD56+ subsets, nor did
CD56+ lymphocytes respond to monocyte-derived
chemokine or thymus-expressed chemokine, the ligands for these
receptors (respectively). Thus, CD56+ subsets may
not be divided into cutaneous or systemic vs mucosal or intestinal
compartments like CD4 T cells (although we cannot completely exclude
the possibility that very small tissue-specialized subsets may exist).
In fact, many CD56+ lymphocytes express both CLA
and 47, a combination
almost never seen on CD4 T cells (J. J. Campbell, unpublished
observations).
Furthermore, the two peripheral blood NK populations investigated in this study (CD16+ and CD16-) do not appear to have any further subdivisions at all, at least in terms of chemokine receptor expression. In this respect, their trafficking profiles may parallel more closely the cells of the innate immune system, whose migration is determined primarily by developmental processes, rather than the Ag-induced homing properties of memory or effector T cells. Like other components of the constitutive immune system in the circulation (such as neutrophils and monocytes), NK cells may be universally attracted to particular areas of inflammation. In fact, this analogy can be taken farther: The chemokine receptor repertoire of CD16+ NK cells is similar to that of neutrophils, and these cells may thus be similarly attracted to sites of acute inflammation. With the exception of CCR7, chemokine receptor expression of CD16- NK cells is more like that of monocytes, and these receptors may serve to bring the cells into sites of more chronic inflammation.
The uniformity of chemokine receptor expression for NK subsets
discussed above is in marked contrast to that of NK-T cells, which are
subdivided into populations that express differing profiles of
chemokine receptors. NK-T cells expressed diverse levels of CCR1, CCR2,
CCR6, CXCR1, and CX3CR1. The number of high and low expressers of each
of these receptors varied greatly among individuals (J. J .Campbell,
unpublished observations). It remains to be seen whether these
differences are related to the inflammatory state, age, or genetics of
the individual. Although NK-T cells are not divided into
tissue-specific subsets along the same lines as CD4 T cells (e.g.,
CLA+/CCR4+ skin-homing and
47high/CCR9+
gut-homing subsets), their subdivisions may imply new, as yet
unrecognized homing cascades to other tissues or organs. In addition,
NK-T cells are the only CD56+ population to
express the orphan chemokine receptor Bonzo (27, 28). In some of the donors (3 of 12), the NK-T population
possessed a subset with 3- to 5-fold higher CD3 expression than the
other NK-T cells. For these donors, Bonzo expression was associated
only with this CD3high population (J. J.
Campbell, unpublished observations).
Homing of CD56+ lymphocytes through lymphoid organs?
CCR7 has recently been shown essential for T cell homing to secondary lymphoid organs through high endothelial venules (29, 30). NK cells are not normally thought to be associated with secondary lymphoid organs, and indeed CD16+ NK cells both lack CCR7 and fail to respond to CCR7 ligands. However, CD16- NK cells express high levels of CCR7, and respond very well to CCR7 ligands. These cells also express very high levels of L-selectin, which is another molecule necessary for homing through high endothelial venule (31). This small subset of NK cells may thus have a role in the events that occur within secondary lymphoid organs, and it will be interesting to see whether these cells can be found in such organs in future studies.
Measuring chemokine-induced enrichment vs direct migration within complex populations
Of all PBLs, NK-T cells were the predominant phenotype attracted
by the CCR5 ligand MIP-1 (Fig. 2, lower left panel).
MIP-1 appears to be a poorly performing chemokine for in vitro
chemotaxis, in comparison with other chemokines. The dramatic effect of
MIP-1 on NK-T vs other lymphocytes may thus not have been detected
unless the relative enrichment numbers had been calculated (Fig. 2),
demonstrating the importance of such an assay in understanding
differential responses to chemokines.
Conclusions
Although CD56+ lymphocytes are derived from multiple lineages, they share a functional association with immunosurveillance and antitumor responses (1, 21, 22). By understanding the pathways by which these cell types traffic throughout the body, we can begin to decipher the mechanisms by which these cells locate and infiltrate neoplasias. Such knowledge may lead to advances in therapy, allowing the design of antitumor cells with the capability of homing to and destroying cancers untreatable with current methods.
In this study, we have performed a comprehensive analysis of
CD56+ PBL subsets. We have found that the
CD16+ and CD16- NK subsets
are very different with respect to each other, but are internally
uniform. We have found that NK-T cells express a large number of
chemokine receptors, and are internally diverse. We have found that
NK-T cells are the predominant responding cell type to the CCR5 ligand
MIP-1. We have found that CD16- NK cells are
the only CD56+ population that uniformly
expresses all of the homing molecules necessary to traffic into
secondary lymphoid organs through high endothelial venule. The
dramatically different chemokine receptor repertoires among these
subsets may thus define entirely different routes of recirculation for
these cells.
Note added in Proof. Since submission of this manuscript, the ligand for Bonzo has been identified as CXCL16 (32, 33), and Bonzo has been accordingly redesignated as CXCR6.
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Footnotes |
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2 Address correspondence and reprint requests to Dr. James J. Campbell, Harvard Medical School, Children’s Hospital, Division of Transfusion Medicine, 300 Longwood Avenue, Room BD-401, Boston, MA 02115. E-mail address: campbell_ja{at}tch.harvard.edu
3 Abbreviations used in this paper: CXCR, CXC chemokine receptor; IP-10, IFN--induced protein-10; ITAC, IFN--inducible T cell chemoattractant; MCP, monocyte chemoattractant protein; MIP, macrophage-inflammatory protein; SDF, stromal-derived factor; SLC, secondary lymphoid tissue chemokine.
Received for publication December 15, 2000. Accepted for publication March 5, 2001.
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F. B. Thoren, A. I. Romero, S. Hermodsson, and K. Hellstrand The CD16-/CD56bright Subset of NK Cells Is Resistant to Oxidant-Induced Cell Death J. Immunol., July 15, 2007; 179(2): 781 - 785. [Abstract] [Full Text] [PDF]
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S. Parolini, A. Santoro, E. Marcenaro, W. Luini, L. Massardi, F. Facchetti, D. Communi, M. Parmentier, A. Majorana, M. Sironi, et al. The role of chemerin in the colocalization of NK and dendritic cell subsets into inflamed tissues Blood, May 1, 2007; 109(9): 3625 - 3632. [Abstract] [Full Text] [PDF]
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C. Romagnani, K. Juelke, M. Falco, B. Morandi, A. D'Agostino, R. Costa, G. Ratto, G. Forte, P. Carrega, G. Lui, et al. CD56brightCD16- Killer Ig-Like Receptor- NK Cells Display Longer Telomeres and Acquire Features of CD56dim NK Cells upon Activation J. Immunol., April 15, 2007; 178(8): 4947 - 4955. [Abstract] [Full Text] [PDF]
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 C. Dunn, M. Brunetto, G. Reynolds, T. Christophides, P. T. Kennedy, P. Lampertico, A. Das, A. R. Lopes, P. Borrow, K. Williams, et al. Cytokines induced during chronic hepatitis B virus infection promote a pathway for NK cell-mediated liver damage J. Exp. Med., March 19, 2007; 204(3): 667 - 680. [Abstract] [Full Text] [PDF]
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M. V. Ramos, G. C. Fernandez, N. Patey, P. Schierloh, R. Exeni, I. Grimoldi, G. Vallejo, C. Elias-Costa, M. del Carmen Sasiain, H. Trachtman, et al. Involvement of the fractalkine pathway in the pathogenesis of childhood hemolytic uremic syndrome Blood, March 15, 2007; 109(6): 2438 - 2445. [Abstract] [Full Text] [PDF]
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 D. B. Keskin, D. S. J. Allan, B. Rybalov, M. M. Andzelm, J. N. H. Stern, H. D. Kopcow, L. A. Koopman, and J. L. Strominger TGFbeta promotes conversion of CD16+ peripheral blood NK cells into CD16- NK cells with similarities to decidual NK cells PNAS, February 27, 2007; 104(9): 3378 - 3383. [Abstract] [Full Text] [PDF]
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 H. Bayer, T. Muller, D. Myrtek, S. Sorichter, M. Ziegenhagen, J. Norgauer, G. Zissel, and M. Idzko Serotoninergic Receptors on Human Airway Epithelial Cells Am. J. Respir. Cell Mol. Biol., January 1, 2007; 36(1): 85 - 93. [Abstract] [Full Text] [PDF]
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R. D. Berahovich, N. L. Lai, Z. Wei, L. L. Lanier, and T. J. Schall Evidence for NK Cell Subsets Based on Chemokine Receptor Expression J. Immunol., December 1, 2006; 177(11): 7833 - 7840. [Abstract] [Full Text] [PDF]
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D. Soler, T. R. Chapman, L. R. Poisson, L. Wang, J. Cote-Sierra, M. Ryan, A. McDonald, S. Badola, E. Fedyk, A. J. Coyle, et al. CCR8 Expression Identifies CD4 Memory T Cells Enriched for FOXP3+ Regulatory and Th2 Effector Lymphocytes J. Immunol., November 15, 2006; 177(10): 6940 - 6951. [Abstract] [Full Text] [PDF]
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 S. Goda, H. Inoue, H. Umehara, M. Miyaji, Y. Nagano, N. Harakawa, H. Imai, P. Lee, J. B. MaCarthy, T. Ikeo, et al. Matrix Metalloproteinase-1 Produced by Human CXCL12-Stimulated Natural Killer Cells Am. J. Pathol., August 1, 2006; 169(2): 445 - 458. [Abstract] [Full Text] [PDF]
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M. Heydtmann, D. Hardie, P. L. Shields, J. Faint, C. D. Buckley, J. J. Campbell, M. Salmon, and D. H. Adams Detailed Analysis of Intrahepatic CD8 T Cells in the Normal and Hepatitis C-Infected Liver Reveals Differences in Specific Populations of Memory Cells with Distinct Homing Phenotypes J. Immunol., July 1, 2006; 177(1): 729 - 738. [Abstract] [Full Text] [PDF]
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D. Huang, F.-D. Shi, S. Jung, G. C. Pien, J. Wang, T. P. Salazar-Mather, T. T. He, J. T. Weaver, H.-G. Ljunggren, C. A. Biron, et al. The neuronal chemokine CX3CL1/fractalkine selectively recruits NK cells that modify experimental autoimmune encephalomyelitis within the central nervous system FASEB J, May 1, 2006; 20(7): 896 - 905. [Abstract] [Full Text] [PDF]
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J. Harcourt, R. Alvarez, L. P. Jones, C. Henderson, L. J. Anderson, and R. A. Tripp Respiratory Syncytial Virus G Protein and G Protein CX3C Motif Adversely Affect CX3CR1+ T Cell Responses J. Immunol., February 1, 2006; 176(3): 1600 - 1608. [Abstract] [Full Text] [PDF]
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 T. Yamaguchi, K. Kitaya, N. Daikoku, T. Yasuo, S. Fushiki, and H. Honjo Potential Selectin L Ligands Involved in Selective Recruitment of Peripheral Blood CD16(-) Natural Killer Cells into Human Endometrium Biol Reprod, January 1, 2006; 74(1): 35 - 40. [Abstract] [Full Text] [PDF]
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P. Schierloh, N. Yokobori, M. Aleman, R. M. Musella, M. Beigier-Bompadre, M. A. Saab, L. Alves, E. Abbate, S. S. de la Barrera, and M. C. Sasiain Increased Susceptibility to Apoptosis of CD56dimCD16+ NK Cells Induces the Enrichment of IFN-{gamma}-Producing CD56bright Cells in Tuberculous Pleurisy J. Immunol., November 15, 2005; 175(10): 6852 - 6860. [Abstract] [Full Text] [PDF]
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J. Hanna, H. Mussaffi, G. Steuer, S. Hanna, M. Deeb, H. Blau, T. I. Arnon, N. Weizman, and O. Mandelboim Functional aberrant expression of CCR2 receptor on chronically activated NK cells in patients with TAP-2 deficiency Blood, November 15, 2005; 106(10): 3465 - 3473. [Abstract] [Full Text] [PDF]
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Y. Sen, B. Yongyi, H. Yuling, X. Luokun, H. Li, X. Jie, D. Tao, Z. Gang, L. Junyan, H. Chunsong, et al. V{alpha}24-Invariant NKT Cells from Patients with Allergic Asthma Express CCR9 at High Frequency and Induce Th2 Bias of CD3+ T Cells upon CD226 Engagement J. Immunol., October 15, 2005; 175(8): 4914 - 4926. [Abstract] [Full Text] [PDF]
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N. Bendriss-Vermare, S. Burg, H. Kanzler, L. Chaperot, T. Duhen, O. de Bouteiller, M. D'agostini, J.-M. Bridon, I. Durand, J. M. Sederstrom, et al. Virus overrides the propensity of human CD40L-activated plasmacytoid dendritic cells to produce Th2 mediators through synergistic induction of IFN-{gamma} and Th1 chemokine production J. Leukoc. Biol., October 1, 2005; 78(4): 954 - 966. [Abstract] [Full Text] [PDF]
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T. Walzer, M. Dalod, S. H. Robbins, L. Zitvogel, and E. Vivier Natural-killer cells and dendritic cells: "l'union fait la force" Blood, October 1, 2005; 106(7): 2252 - 2258. [Abstract] [Full Text] [PDF]
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X. Wu, L.-P. Jin, M.-M. Yuan, Y. Zhu, M.-Y. Wang, and D.-J. Li Human First-Trimester Trophoblast Cells Recruit CD56brightCD16- NK Cells into Decidua by Way of Expressing and Secreting of CXCL12/Stromal Cell-Derived Factor 1 J. Immunol., July 1, 2005; 175(1): 61 - 68. [Abstract] [Full Text] [PDF]
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 M. J. van den Heuvel, J. Horrocks, S. Bashar, K. Hatta, S. Burke, S. S. Evans, B. A. Croy, and F. R. Tekpetey Periovulatory Increases in Tissue Homing Potential of Circulating CD56bright Cells Are Associated with Fertile Menstrual Cycles J. Clin. Endocrinol. Metab., June 1, 2005; 90(6): 3606 - 3613. [Abstract] [Full Text] [PDF]
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 L. Dyugovskaya, P. Lavie, M. Hirsh, and L. Lavie Activated CD8+ T-lymphocytes in obstructive sleep apnoea Eur. Respir. J., May 1, 2005; 25(5): 820 - 828. [Abstract] [Full Text] [PDF]
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K. Kitaya, T. Yamaguchi, and H. Honjo Central Role of Interleukin-15 in Postovulatory Recruitment of Peripheral Blood CD16(-) Natural Killer Cells into Human Endometrium J. Clin. Endocrinol. Metab., May 1, 2005; 90(5): 2932 - 2940. [Abstract] [Full Text] [PDF]
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M. J. van den Heuvel, J. Horrocks, S. Bashar, S. Taylor, S. Burke, K. Hatta, J. E. Lewis, and B. A. Croy Menstrual Cycle Hormones Induce Changes in Functional Interactions between Lymphocytes and Decidual Vascular Endothelial Cells J. Clin. Endocrinol. Metab., May 1, 2005; 90(5): 2835 - 2842. [Abstract] [Full Text] [PDF]
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Z. Li, W. K. Lim, S. P. Mahesh, B. Liu, and R. B. Nussenblatt Cutting Edge: In Vivo Blockade of Human IL-2 Receptor Induces Expansion of CD56bright Regulatory NK Cells in Patients with Active Uveitis J. Immunol., May 1, 2005; 174(9): 5187 - 5191. [Abstract] [Full Text] [PDF]
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A. Deng, S. Chen, Q. Li, S.-c. Lyu, C. Clayberger, and A. M. Krensky Granulysin, a Cytolytic Molecule, Is Also a Chemoattractant and Proinflammatory Activator J. Immunol., May 1, 2005; 174(9): 5243 - 5248. [Abstract] [Full Text] [PDF]
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A. Saudemont, N. Jouy, D. Hetuin, and B. Quesnel NK cells that are activated by CXCL10 can kill dormant tumor cells that resist CTL-mediated lysis and can express B7-H1 that stimulates T cells Blood, March 15, 2005; 105(6): 2428 - 2435. [Abstract] [Full Text] [PDF]
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M. Heydtmann, P. F. Lalor, J. A. Eksteen, S. G. Hubscher, M. Briskin, and D. H. Adams CXC Chemokine Ligand 16 Promotes Integrin-Mediated Adhesion of Liver-Infiltrating Lymphocytes to Cholangiocytes and Hepatocytes within the Inflamed Human Liver J. Immunol., January 15, 2005; 174(2): 1055 - 1062. [Abstract] [Full Text] [PDF]
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N. J. Hannan, R. L. Jones, H. O. D. Critchley, G. J. Kovacs, P. A. W. Rogers, B. Affandi, and L. A. Salamonsen Coexpression of Fractalkine and Its Receptor in Normal Human Endometrium and in Endometrium from Users of Progestin-Only Contraception Supports a Role for Fractalkine in Leukocyte Recruitment and Endometrial Remodeling J. Clin. Endocrinol. Metab., December 1, 2004; 89(12): 6119 - 6129. [Abstract] [Full Text] [PDF]
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R. L. Jones, N. J. Hannan, T. J. Kaitu'u, J. Zhang, and L. A. Salamonsen Identification of Chemokines Important for Leukocyte Recruitment to the Human Endometrium at the Times of Embryo Implantation and Menstruation J. Clin. Endocrinol. Metab., December 1, 2004; 89(12): 6155 - 6167. [Abstract] [Full Text] [PDF]
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J. Hanna, P. Bechtel, Y. Zhai, F. Youssef, K. McLachlan, and O. Mandelboim Novel Insights on Human NK Cells' Immunological Modalities Revealed by Gene Expression Profiling J. Immunol., December 1, 2004; 173(11): 6547 - 6563. [Abstract] [Full Text] [PDF]
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C. L. Sentman, S. K. Meadows, C. R. Wira, and M. Eriksson Recruitment of Uterine NK Cells: Induction of CXC Chemokine Ligands 10 and 11 in Human Endometrium by Estradiol and Progesterone J. Immunol., December 1, 2004; 173(11): 6760 - 6766. [Abstract] [Full Text] [PDF]
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G. Ferlazzo, M. Pack, D. Thomas, C. Paludan, D. Schmid, T. Strowig, G. Bougras, W. A. Muller, L. Moretta, and C. Munz Distinct roles of IL-12 and IL-15 in human natural killer cell activation by dendritic cells from secondary lymphoid organs PNAS, November 23, 2004; 101(47): 16606 - 16611. [Abstract] [Full Text] [PDF]
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 J. Barlic, D. H. McDermott, M. N. Merrell, J. Gonzales, L. E. Via, and P. M. Murphy Interleukin (IL)-15 and IL-2 Reciprocally Regulate Expression of the Chemokine Receptor CX3CR1 through Selective NFAT1- and NFAT2-dependent Mechanisms J. Biol. Chem., November 19, 2004; 279(47): 48520 - 48534. [Abstract] [Full Text] [PDF]
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N. Dalbeth, R. Gundle, R. J. O. Davies, Y. C. G. Lee, A. J. McMichael, and M. F. C. Callan CD56bright NK Cells Are Enriched at Inflammatory Sites and Can Engage with Monocytes in a Reciprocal Program of Activation J. Immunol., November 15, 2004; 173(10): 6418 - 6426. [Abstract] [Full Text] [PDF]
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C. Borg, A. Jalil, D. Laderach, K. Maruyama, H. Wakasugi, S. Charrier, B. Ryffel, A. Cambi, C. Figdor, W. Vainchenker, et al. NK cell activation by dendritic cells (DCs) requires the formation of a synapse leading to IL-12 polarization in DCs Blood, November 15, 2004; 104(10): 3267 - 3275. [Abstract] [Full Text] [PDF]
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E. Lavergne, C. Combadiere, M. Iga, A. Boissonnas, O. Bonduelle, M. Maho, P. Debre, and B. Combadiere Intratumoral CC Chemokine Ligand 5 Overexpression Delays Tumor Growth and Increases Tumor Cell Infiltration J. Immunol., September 15, 2004; 173(6): 3755 - 3762. [Abstract] [Full Text] [PDF]
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S. Sivori, M. Falco, M. D. Chiesa, S. Carlomagno, M. Vitale, L. Moretta, and A. Moretta CpG and double-stranded RNA trigger human NK cells by Toll-like receptors: Induction of cytokine release and cytotoxicity against tumors and dendritic cells PNAS, July 6, 2004; 101(27): 10116 - 10121. [Abstract] [Full Text] [PDF]
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K. Kitaya, T. Nakayama, N. Daikoku, S. Fushiki, and H. Honjo Spatial and Temporal Expression of Ligands for CXCR3 and CXCR4 in Human Endometrium J. Clin. Endocrinol. Metab., May 1, 2004; 89(5): 2470 - 2476. [Abstract] [Full Text] [PDF]
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G. Ferlazzo and C. Munz NK Cell Compartments and Their Activation by Dendritic Cells J. Immunol., February 1, 2004; 172(3): 1333 - 1339. [Full Text] [PDF]
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G. Ferlazzo, D. Thomas, S.-L. Lin, K. Goodman, B. Morandi, W. A. Muller, A. Moretta, and C. Munz The Abundant NK Cells in Human Secondary Lymphoid Tissues Require Activation to Express Killer Cell Ig-Like Receptors and Become Cytolytic J. Immunol., February 1, 2004; 172(3): 1455 - 1462. [Abstract] [Full Text] [PDF]
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E. S. Doubrovina, M. M. Doubrovin, E. Vider, R. B. Sisson, R. J. O'Reilly, B. Dupont, and Y. M. Vyas Evasion from NK Cell Immunity by MHC Class I Chain-Related Molecules Expressing Colon Adenocarcinoma J. Immunol., December 15, 2003; 171(12): 6891 - 6899. [Abstract] [Full Text] [PDF]
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J. Barlic, J. M. Sechler, and P. M. Murphy IL-15 and IL-2 oppositely regulate expression of the chemokine receptor CX3CR1 Blood, November 15, 2003; 102(10): 3494 - 3503. [Abstract] [Full Text] [PDF]
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L. A. Koopman, H. D. Kopcow, B. Rybalov, J. E. Boyson, J. S. Orange, F. Schatz, R. Masch, C. J. Lockwood, A. D. Schachter, P. J. Park, et al. Human Decidual Natural Killer Cells Are a Unique NK Cell Subset with Immunomodulatory Potential J. Exp. Med., October 20, 2003; 198(8): 1201 - 1212. [Abstract] [Full Text] [PDF]
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K. Beider, A. Nagler, O. Wald, S. Franitza, M. Dagan-Berger, H. Wald, H. Giladi, S. Brocke, J. Hanna, O. Mandelboim, et al. Involvement of CXCR4 and IL-2 in the homing and retention of human NK and NK T cells to the bone marrow and spleen of NOD/SCID mice Blood, September 15, 2003; 102(6): 1951 - 1958. [Abstract] [Full Text] [PDF]
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J. Hanna, O. Wald, D. Goldman-Wohl, D. Prus, G. Markel, R. Gazit, G. Katz, R. Haimov-Kochman, N. Fujii, S. Yagel, et al. CXCL12 expression by invasive trophoblasts induces the specific migration of CD16- human natural killer cells Blood, September 1, 2003; 102(5): 1569 - 1577. [Abstract] [Full Text] [PDF]
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A. A. Maghazachi G protein-coupled receptors in natural killer cells J. Leukoc. Biol., July 1, 2003; 74(1): 16 - 24. [Abstract] [Full Text] [PDF]
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T. A. Fehniger, M. A. Cooper, G. J. Nuovo, M. Cella, F. Facchetti, M. Colonna, and M. A. Caligiuri CD56bright natural killer cells are present in human lymph nodes and are activated by T cell-derived IL-2: a potential new link between adaptive and innate immunity Blood, April 15, 2003; 101(8): 3052 - 3057. [Abstract] [Full Text] [PDF]
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K. Kitaya, T. Nakayama, T. Okubo, H. Kuroboshi, S. Fushiki, and H. Honjo Expression of Macrophage Inflammatory Protein-1{beta} in Human Endometrium: Its Role in Endometrial Recruitment of Natural Killer Cells J. Clin. Endocrinol. Metab., April 1, 2003; 88(4): 1809 - 1814. [Abstract] [Full Text] [PDF]
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R. Castriconi, C. Cantoni, M. Della Chiesa, M. Vitale, E. Marcenaro, R. Conte, R. Biassoni, C. Bottino, L. Moretta, and A. Moretta Transforming growth factor beta 1 inhibits expression of NKp30 and NKG2D receptors: Consequences for the NK-mediated killing of dendritic cells PNAS, April 1, 2003; 100(7): 4120 - 4125. [Abstract] [Full Text] [PDF]
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A. Gismondi, J. Jacobelli, R. Strippoli, F. Mainiero, A. Soriani, L. Cifaldi, M. Piccoli, L. Frati, and A. Santoni Proline-Rich Tyrosine Kinase 2 and Rac Activation by Chemokine and Integrin Receptors Controls NK Cell Transendothelial Migration J. Immunol., March 15, 2003; 170(6): 3065 - 3073. [Abstract] [Full Text] [PDF]
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D. Soler, T. L. Humphreys, S. M. Spinola, and J. J. Campbell CCR4 versus CCR10 in human cutaneous TH lymphocyte trafficking Blood, March 1, 2003; 101(5): 1677 - 1682. [Abstract] [Full Text] [PDF]
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M. Honczarenko, Y. Le, A. M. Glodek, M. Majka, J. J. Campbell, M. Z. Ratajczak, and L. E. Silberstein CCR5-binding chemokines modulate CXCL12 (SDF-1)-induced responses of progenitor B cells in human bone marrow through heterologous desensitization of the CXCR4 chemokine receptor Blood, September 18, 2002; 100(7): 2321 - 2329. [Abstract] [Full Text] [PDF]
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D. L. Hodge, W. B. Schill, J. M. Wang, I. Blanca, D. A. Reynolds, J. R. Ortaldo, and H. A. Young IL-2 and IL-12 Alter NK Cell Responsiveness to IFN-{gamma}-Inducible Protein 10 by Down-Regulating CXCR3 Expression J. Immunol., June 15, 2002; 168(12): 6090 - 6098. [Abstract] [Full Text] [PDF]
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M. Nishimura, H. Umehara, T. Nakayama, O. Yoneda, K. Hieshima, M. Kakizaki, N. Dohmae, O. Yoshie, and T. Imai Dual Functions of Fractalkine/CX3C Ligand 1 in Trafficking of Perforin+/Granzyme B+ Cytotoxic Effector Lymphocytes That Are Defined by CX3CR1 Expression J. Immunol., June 15, 2002; 168(12): 6173 - 6180. [Abstract] [Full Text] [PDF]
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L. Zitvogel Dendritic and Natural Killer Cells Cooperate in the Control/Switch of Innate Immunity J. Exp. Med., February 4, 2002; 195(3): F9 - F14. [Full Text] [PDF]
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M. J. Robertson Role of chemokines in the biology of natural killer cells J. Leukoc. Biol., February 1, 2002; 71(2): 173 - 183. [Abstract] [Full Text] [PDF]
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K. Red-Horse, P. M. Drake, M. D. Gunn, and S. J. Fisher Chemokine Ligand and Receptor Expression in the Pregnant Uterus : Reciprocal Patterns in Complementary Cell Subsets Suggest Functional Roles Am. J. Pathol., December 1, 2001; 159(6): 2199 - 2213. [Abstract] [Full Text] [PDF]
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J. Dunne, S. Lynch, C. O'Farrelly, S. Todryk, J. E. Hegarty, C. Feighery, and D. G. Doherty Selective Expansion and Partial Activation of Human NK Cells and NK Receptor-Positive T Cells by IL-2 and IL-15 J. Immunol., September 15, 2001; 167(6): 3129 - 3138. [Abstract] [Full Text] [PDF]
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A. Motsinger, D. W. Haas, A. K. Stanic, L. Van Kaer, S. Joyce, and D. Unutmaz CD1d-restricted Human Natural Killer T Cells Are Highly Susceptible to Human Immunodeficiency Virus 1 Infection J. Exp. Med., April 1, 2002; 195(7): 869 - 879. [Abstract] [Full Text] [PDF]
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,
CD56+/CD16+/CD3-; 
,
CD56+/CD16-/CD3-; 
,
CD56+/CD3+. Results shown are from one donor,
with all assays performed in parallel on the same day. Results at
optimal concentration are representative of those obtained from 12
donors.