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1  long-lived than canonical, immunoregulatory NK cells.
2 ion of virus-infected and cancerous cells by NK cells.
3 owever, much less is known about its role in NK cells.
4  in CD16a(-) NK cells compared with CD16a(+) NK cells.
5  optimally stimulate IFN-gamma production by NK cells.
6 t one third the capacity of Zap70(hi)Syk(hi) NK cells.
7 C in response to both oligomerised TRAIL and NK cells.
8 sinophils, neutrophils, dendritic cells, and NK cells.
9 roid cancers linked to cytotoxic T cells and NK cells.
10 ented macrophages fully activated autologous NK cells.
11 s with high pretransplant levels of NKG2C(+) NK cells.
12 is critical for maximal TNF-alpha release by NK cells.
13 t or target metastatic disease by harnessing NK cells.
14 ess to allow for effective serial killing of NK cells.
15 r dependencies as compared with conventional NK cells.
16 ce markers, including CD56(hi) and CD56(low) NK cells.
17 +) double-producing CD4, CD8, gammadelta and NK cells.
18  activating receptors expressed by all human NK cells.
19  cooperate in regulating NKG2D expression in NK cells.
20 he lung as bona fide tissue-resident CD69(+) NK cells.
21 results in reduced tumor-killing capacity by NK cells.
22 lls, monocytes, B cells, and natural killer (NK) cells.
23 hat limits the maturation of natural killer (NK) cells.
24 g interferon gamma-producing natural killer (NK) cells.
25 ILRB1-expressing B cells and natural killer (NK) cells.
26 expressed on activated T and natural killer (NK) cells.
27 acting against the virus are Natural Killer (NK) cells.
28  cells including T cells and natural killer (NK) cells.
29 cells vulnerable to lysis by natural killer (NK) cells.
30 al grafts, containing high numbers of mature NK cells, according to PT-Cy-based protocols in 2 indepe
31 ll phenotype, consistent with restoration of NK cell activating and inhibitory receptor repertoire to
32 arget cells led to a significant increase in NK cell activation against said target cells.
33                                        Using NK cell activation and NK cytotoxicity assays, we compar
34 vels a prominent role for the CD16-dependent NK cell activation pathway in the complex array of facto
35     However, although NKp65 utilizes Syk for NK cell activation, a physical association of Syk with t
36 ab) at concentrations that triggered similar NK cell activation, indicating that cell-associated gp35
37 -glucuronidase heparanase that increase upon NK cell activation.
38           Since inhibitory receptors control NK-cell activation and are necessary for MHC-I-dependent
39 objective was to determine the difference in NK cell activity between subjects with vs without CRC.
40 gest a feedback inhibition of IL-15-mediated NK cell activity by IL-32alpha.
41                                The extent of NK cell activity during the innate immune response affec
42 oscopy as the reference standard, a test for NK cell activity in whole blood samples identified patie
43                    Combining natural killer (NK) cell adoptive transfer with hypomethylating agents (
44  and rapid production of interferon-gamma by NK cells after challenge.
45 y of infusing high doses of ex vivo-expanded NK cells after haploidentical HSCT without adverse effec
46                        Donor natural killer (NK) cell alloreactivity in HCT can control leukemic rela
47 cognized by killer cell Ig-like receptors of NK cells, allotypes having the C1 epitope also recognize
48 ed the phenotype of myeloid cells, increased NK cell and Th1 cytokine levels, and reduced immature my
49 d TNF-alpha responses and have low levels of NK cells and CD4(+) and CD8(+) T cells compared to a res
50  Further, proportions of activated cytotoxic NK cells and CD8+ T cells increased significantly during
51 at rmIFN induces the activation of T, B, and NK cells and exhibits antiviral, antiproliferative, and
52 erbates the severity of sepsis by activating NK cells and facilitating IFN-gamma production.
53  expressed by CD56(dim) but not CD56(bright) NK cells and is confined to fully mature NK cells charac
54 eting autophagy on the tumor infiltration by NK cells and its benefit as a novel therapeutic approach
55 ignaling molecule expressed predominantly on NK cells and memory CD8(+) T cells that has been shown t
56                mCD48 expression on B, T, and NK cells and monocytes in severe asthma was significantl
57 l death and survival pathways and implicated NK cells and neutrophil populations in this differential
58                 The distribution of NKG2C(+) NK cells and NKG2C genotypes (NKG2C(+/+), NKG2C(+/del),
59 vo restored perforin expression in CD56(dim) NK cells and partially restored NK cell cytotoxic functi
60      NKG2D is a major activating receptor of NK cells and plays a critical role in tumor immunosurvei
61 ection had significant deficiencies of T and NK cells and poor functional outcomes.
62 sion in Ifitm3-/- mice triggered the loss of NK cells and subsequently impaired control of MCMV repli
63 ls into the tumors including neutrophils and NK cells and suppressed tumor progression.
64 he former treatment activates nature killer (NK) cells and NK T cells, which partially enhances the i
65  that overlaps with those of natural killer (NK) cells and other ILCs.
66 opment and function of human natural killer (NK) cells and T cell subsets limit the applicability of
67 NS2, expression of the S1P receptor S1PR5 on NK cells, and expression of the chemokine receptor CXCR4
68  of cytotoxic T lymphocytes, natural killer (NK) cells, and macrophages resulting in hypercytokinemia
69  Most importantly, only DAC potentiated HSPC-NK cell anti-leukemic activity in vivo.
70                 Our findings show that human NK cells are able to terminate their functional activity
71  these studies indicate that tissue-resident NK cells are evolutionarily conserved in humans and mice
72                                              NK cells are highly efficient at preventing cancer metas
73 ts indirectly support that adaptive NKG2C(+) NK cells are involved in the control of CMV in KTRs.
74 onsequences of the cross-talk between M1 and NK cells are known, the outcome of the cross-talk betwee
75     Moreover, our data suggest that adaptive NK cells are more long-lived than canonical, immunoregul
76                                              NK cells are part of the innate immune system, and are a
77        In this article, we show that uterine NK cells are the key source of IL-10 that is required to
78 umanized mice indicating that human CD49e(-) NK cells are tissue resident in the liver.
79                              Natural killer (NK) cells are located at the periphery of the lymph node
80           These findings identify CD56bright NK cells as potent antitumor effectors that warrant furt
81          Maturation of human natural killer (NK) cells as defined by accumulation of cell-surface exp
82 atherosclerosis, it is not yet clear whether NK cells behave as protective or proatherogenic effector
83 Exposure to IL12 rescued the cytotoxicity of NK cells but also led to the emergence of an immature NK
84  following RG-101 injection, suggesting that NK cells, but not HCV adaptive immunity, may contribute
85                                  Activity of NK cells can be measured in a small volume of whole bloo
86 o, it remains unknown whether these expanded NK cells can persist and/or proliferate in vivo in the a
87  To test the hypothesis that natural killer (NK) cells can decrease the risk of leukemia relapse, we
88 -alpha, and IL-12, as well as recruitment of NK cells, CD11b(+), and CD11c(+) cells in the lung.
89 with biopsies with AMR provides evidence for NK cell CD16a activation in AMR.
90                                           In NK cells, CD16a stimulation induced increased expression
91 nduce selective fratricide of SLAMF7(+/high) NK cells, CD4(+) and CD8(+) T cells, and B cells.
92 eukin-15 present in patients' sera, immature NK cells (CD62L(+)NKG2A(+)KIR(-)) became highly prevalen
93 of bacterial foci to attract macrophages and NK cells, cell types known to be important for early def
94 ht) NK cells and is confined to fully mature NK cells characterized by the NKG2A(-)KIR(+)CD57(+) phen
95  can furthermore activate primary KIR2DS1(+) NK cell clones.
96 ise mechanism underlying this synergy within NK cell clusters remains unclear.
97 er degranulation and cytotoxic activity than NK cells cocultured with M1.
98                              Also, CD56(dim) NK cells cocultured with M2 displayed lower degranulatio
99 er, miR-218 was highly expressed in CD16a(-) NK cells compared with CD16a(+) NK cells.
100  gene turnover of trans-membrane proteins in NK cells compared with T cells in fish species, suggesti
101 eady harbor significantly altered T cell and NK cell compartments.
102 e for NKG2D-ligand interaction via homotypic NK cell contact in NK cell effector function.
103 t induce the Zap70(low)Syk(low) phenotype in NK cells: continuous stimulation with activation beads a
104 in CD56(dim) NK cells and partially restored NK cell cytotoxic function.
105 sceptibility of cisplatin-resistant cells to NK cell cytotoxicity when neutralizing antibody of PD-1
106                              Natural killer (NK)-cell cytotoxicity assays can quickly screen for all
107                                              NK cell deficiency can result in severe or refractory vi
108 growth retardation, chronic neutropenia, and NK cell deficiency.
109 growth retardation, chronic neutropenia, and NK cell deficiency.
110 ciated with myeloid, B-, and natural killer (NK)-cell deficiency.
111 gnature of genes present in mouse ILC except NK cells, defined by Immunological Genome Project studie
112                               Interestingly, NK cell depletion experiments demonstrated a critical cu
113 re deficient in IL-18 production, and lacked NK cell-derived IFN-gamma.
114                                              NK cells develop from hematopoietic stem cells, and few
115 monogenic errors that specifically interrupt NK cell development have been reported.
116 we show that STAT5 dimers are sufficient for NK cell development, whereas STAT5 tetramers mediate NK
117             DNAM-1 is expressed early during NK-cell development, precedes the expression of MHC-I-sp
118    The recent discoveries of tissue-resident NK cell developmental intermediates, non-NK innate lymph
119    Supporting this hypothesis, proliferating NK cells did not express aldehyde dehydrogenase and were
120 eage-negative progenitors displayed impaired NK-cell differentiation.
121                Additionally, we observe that NK cells display a more heterogeneous range of migratory
122 e cerebral artery occlusion, natural killer (NK) cells display remarkably distinct temporal and trans
123  loads without a marked CD8 lymphocytosis or NK cell disturbance like those seen in patients during t
124  13 patients enrolled received all 3 planned NK-cell doses (1 x 10(5)/kg to 1 x 10(8)/kg per dose).
125                        Here we characterized NK cell dynamics in 17 patients who received unmanipulat
126 d uncover how cytokine stimulation overcomes NK cell education.
127                  We propose a model in which NK-cell education prevents or delays downregulation of D
128 hether DNAM-1 expression is also involved in NK-cell education.
129 virus (MCMV)-encoded protein, m12, restrains NK cell effector function by directly engaging the inhib
130 interaction via homotypic NK cell contact in NK cell effector function.
131 h as CCL3, CCL4, and XCL1, and modulators of NK cell effector functions (TNFRSF9, CRTAM, CD160).
132 iently generate large quantities of expanded NK cells ex vivo, it remains unknown whether these expan
133         Moreover, resting cord blood KIR3DL1 NK cells exhibited a basal alloreactivity against Bw4 ta
134          When exposed to human cancer cells, NK cell expanded ex vivo in the presence of a GSK3 inhib
135 , 6, 12, and 24 mo), posttransplant NKG2C(+) NK cell expansions were not observed in every patient wi
136 trated that freshly isolated mouse and human NK cells express low levels of the endo-beta-D-glucuroni
137 ctivation with IL-12, IL-15, and IL-18 human NK cells express NKG2D ligands of the UL16 binding prote
138                              Natural killer (NK) cells express MHC class I (MHC-I)-specific receptors
139                        Adult natural killer (NK) cells express only IL2Rbeta and IL2Rgamma subunits a
140  this Zap70(low)Syk(low) subset consisted of NK cells expressing a range of surface markers, includin
141 ion of NK-cell proportions and a decrease of NK cells expressing activation receptors; however, the m
142 characterized a novel subpopulation of human NK cells expressing high levels of PD-1.
143 rowth, whereas intestinal Rorc(fm-) ILC1s or NK cells fail to inhibit tumor progression.
144 lation with target cells, Zap70(low)Syk(low) NK cells failed to produce IFN-gamma and lysed target ce
145                  Adaptive (NKG2C(+) CD57(+)) NK cell features were not associated with reservoir size
146 hus, during GVHD, donor T cells compete with NK cells for IL-15 thereby inducing profound defects in
147                             Peripheral blood NK cells from individuals with GATA2 mutation proliferat
148 ing the release of large lytic granules from NK cells from patients with CHS and could be a novel tar
149 eover, consistent with an adaptive identity, NK cells from patients with GATA2 mutation displayed alt
150                             Peripheral blood NK cells from patients with STAT1 GOF mutations had impa
151                                              NK cells from patients with STAT1 GOF mutations were tre
152 wnregulate NKG2D in response to VPA, but not NK cells from STAT3 knockout mice.
153                                              NK cells from STAT3 wild-type mice downregulate NKG2D in
154 or genetic ablation of innervation preserved NK cell function and restrained post-stroke infection.
155   The phenotype was accompanied by deficient NK cell function and was stable over time.
156 levels of IL-18 and a complete abrogation of NK cell function in HSV-2 infection.
157 ctivation is crucial in regulating pulmonary NK cell function, and suggest that NK cells serve to lim
158 PD-L1, and PD-L2, molecules that might limit NK cell function.
159 molecules, and the consequences for KIR2DS1+ NK-cell function.
160 itabine (DAC) in combination with allogeneic NK cells generated from CD34(+) hematopoietic stem and p
161       Particularly, the adoptive transfer of NK cells has garnered attention due to their natural cyt
162                                              NK cells have been reported to respond against EBV-infec
163 te-of-the-art mouse models, demonstrate that NK cells have no direct effect on the natural developmen
164                 Classically, natural killer (NK) cells have been defined by nonspecific innate killin
165                              Natural killer (NK) cells have long been considered short-lived effector
166 ine IL-15, which is important for T cell and NK cell homeostasis.
167 importance of STAT5 tetramers in maintaining NK cell homoeostasis.
168 ver, mice lacking heparanase specifically in NK cells (Hpsefl/fl NKp46-iCre mice) were highly tumor p
169 ed Rorc(fm+) ILCs acquire an natural killer (NK) cell/ILC1-like phenotype.
170 etramer formation could represent a cause of NK cell immunodeficiency, and interrupting STAT5 tetrame
171 nced survival and effector function of human NK cells in a B-cell acute lymphoblastic leukemia xenotr
172 e studies point to a unique role for CD57(+) NK cells in cancer immunosurveillance, yet there is scan
173  support the application of ex vivo expanded NK cells in cancer immunotherapy and provide a translati
174 ice indicate the presence of tissue-resident NK cells in certain organs, such as the liver, that disp
175 endent cell cytotoxic activity of peripheral NK cells in HT recipients were evaluated using a noninva
176 ase, thereby emphasizing a critical role for NK cells in human antiviral defense.
177 D16(+) NK cells made up the vast majority of NK cells in human lungs, had a more differentiated pheno
178 e cells that represent a broader category of NK cells in mucosal and non-mucosal pathological tissues
179 ne and characterised by the absence of T and NK cells in patients.
180  immunoglobulin-like receptors compared with NK cells in peripheral blood.
181  an IL-2R alpha chain, and lytic granules of NK cells in social microwells were polarized toward MTOC
182 immunodeficient Il2rg(-/-) (NSG) mice, human NK cells in SRG-15 mice did not require preactivation bu
183 ata suggest a model in which the majority of NK cells in the human lung dynamically move between bloo
184 tudies of what are now known as conventional NK cells in the mouse spleen or human peripheral blood.
185 otoxic/proinflammatory CD8+ T, NKT-like, and NK cells in the small airways.
186 dinated activation of T and natural killier (NK) cells in addition to gemcitabine chemotherapy to pre
187 e evaluated the functions of natural killer (NK) cells in experimental animal models of atheroscleros
188 sis, discuss the key role of natural killer (NK) cells in the control of metastatic dissemination, an
189 ematopoietic stem and progenitor cells (HSPC-NK cells) in in vitro and in vivo AML models.
190 s showed that neutrophils are involved in an NK cell increase in the synovium, possibly by expressing
191 gand interaction between cytokine-stimulated NK cells increases the activity of the metalloprotease T
192 D16A-expressing Jurkat T cells, degranulated NK cells, induced cytokine production and killed Env-exp
193                               Neutrophil and NK cell infiltration and capillary thrombosis were also
194 bound interleukin 21 (mbIL21) expanded donor NK cells infused before and after haploidentical HSCT fo
195 g stimuli and regulates the surface level of NK-cell inhibitory receptors.
196  numbers, whereas transfer of CD3(-)NK1.1(+) NK cells into the airways of WT hosts suppressed the inf
197 nduction of EBI3 protein expression in mouse NK cells is a late activation event.
198                            Most knowledge on NK cells is based on studies of what are now known as co
199                          NKG2D expression in NK cells is inhibited by the histone deacetylase (HDAC)
200 of normal articular chondrocytes to lysis by NK cells is modulated by NKR-P1A/LLT1 interactions.
201 l and posttranscriptional CD16 expression in NK cells is unknown.
202  lymphoid cells (ILC1s) from natural killer (NK) cells is a gene signature indicative of 'imprinting'
203 otherapy for metastases was compromised when NK cells lacked heparanase.
204              Indeed, after transduction, the NK cell line NK-92 became TCR positive and reacted again
205 acking classical B-, T-, and natural killer (NK)-cell lineage markers (Lin(-)IELs) in the duodenum.
206                                              NK cell lines expressing patients' mutations were genera
207 emokine receptor CXCR4 were all required for NK cell localization during homeostasis and rapid produc
208                              Natural killer (NK) cells localize in the microcirculation in antibody-m
209                                              NK cell lymphoma (NKCL) did not express significant leve
210                             CD56(dim)CD16(+) NK cells made up the vast majority of NK cells in human
211            Furthermore, the IL-10 expressing NK cells markedly enhanced angiogenic responses and plac
212 eport that IL-1R8 serves as a checkpoint for NK cell maturation and effector function.
213 development, whereas STAT5 tetramers mediate NK cell maturation and the expression of maturation-asso
214 naling as an intrinsic negative regulator of NK-cell maturation and antitumor immune responses.
215 n, expansion, and adoptive transfer of these NK cells may allow monitoring of treatment efficacy and
216 d CD94, suggests that CD8+ T cells and CD94+ NK cells may play a major role in AIM.
217 s targeting the V1V2 domain induce up to 60% NK cell mediated lysis of HIV-1 infected PBMCs in a phys
218 les PD-1, Lag-3, and TIGIT, thereby limiting NK cell-mediated control of pulmonary metastases.
219 or-ligand pairs and are thought to allow for NK cell-mediated immunosurveillance of stressed or infec
220 data have been followed by demonstrations of NK cell memory of viruses and viral antigens in mice and
221  can greatly enhance the mature character of NK cells most desired for effective cancer immunotherapy
222 CMV-Th) T cell activity, and natural killer (NK) cell number were measured by flow cytometry.
223 d was associated with significantly improved NK-cell number and function, lower viral infections, and
224 e development of septic shock by maintaining NK cell numbers and integrity.
225  leads to splenic atrophy and contraction of NK cell numbers in the periphery through a modulated exp
226 time in CD8(+) T cells, but not with that in NK cells, of the patients.
227 fied endotoxin shock, which was prevented by NK cell or IFN-gamma depletion.
228 is modulation disappears in mice depleted of NK cells or lacking IFN-gamma, and was mimicked by exoge
229 for normal function of cytotoxic T cells and NK cells) or secondary (resulting from a malignant, infe
230  demonstrated sustained CD3(+), CD19(+), and NK-cell output 15 years post-HSCT.
231  may play a role when an additional systemic NK-cell overactivation occurs.
232 eases, facilitating treatment, but combining NK-cell perforin expression and CD107a upregulation test
233 had a more mature, cytolytic CD57(+)CD62L(-) NK cell phenotype, consistent with restoration of NK cel
234                              Natural killer (NK) cells play a key role in innate immunity by detectin
235 but also led to the emergence of an immature NK cell population that expressed high levels of the coi
236 port the existence of a long-lived, adaptive NK-cell population maintained independently from GPI(pos
237     Mouse liver contains two natural killer (NK) cell populations, one of which recirculates while th
238 tage of effector T cells and natural killer (NK) cells present in the lung.
239 continuous long-term imaging and tracking of NK cell progenitors undergoing in vitro differentiation.
240 h RG-101 is associated with a restoration of NK-cell proportions and a decrease of NK cells expressin
241  depletion efficacy, with low-level residual NK cells providing sufficient help to allow optimal CD8
242 te that mTOR acts as a molecular rheostat of NK cell reactivity controlled by educating receptors and
243  mTOR resulted in a proportional decrease in NK cell reactivity.
244  peptide-dependent binding of the activating NK cell receptor KIR2DS1, providing new insights into th
245 ions in self and non-self ligands via paired NK cell receptors (NKRs).
246                              Natural killer (NK) cells recognize and kill cancer cells and infected c
247 r IL-15 thereby inducing profound defects in NK-cell reconstitution that compromise both leukemia and
248 lass Ia leader sequence-derived peptides for NK cell regulation.
249 the mechanisms of chondrocyte recognition by NK cells remain poorly understood.
250 the outcome of the cross-talk between M2 and NK cells remains ill-defined.
251     Together, these data indicate that human NK cells require IRF8 for development and functional mat
252 iviral therapy, suggesting that the adaptive NK cell response may be inversely related with the degre
253       Analyzing human innate-like T cell and NK cell responses following infection with Plasmodium ha
254 linergic innervation-mediated suppression of NK cell responses in the brain involves RUNX3.
255                                 Depletion of NK cells restored the allergen responsiveness in the lun
256   Notably, A2AR-deficient, terminally mature NK cells retained proliferative capacity and exhibited h
257 -L1/PD-1 agents in enhancing natural killer (NK) cell's function remains largely unknown.
258        PDGF-DD engagement of NKp44 triggered NK cell secretion of interferon gamma (IFN)-gamma and tu
259           The association of CD16a-inducible NK cell-selective transcripts CD160 and XCL1 with biopsi
260         We hypothesized that CD16a-inducible NK cell-selective transcripts would be expressed in huma
261 pulmonary NK cell function, and suggest that NK cells serve to limit ILC2 activation and subsequent a
262                                      Infused NK cells showed sustained expression of most activating
263 D mice, which have a deficiency in T, B, and NK cells, showed minimal disease at cutaneous sites but
264                       Functional analysis of NK cells shows a significant impairment of cytolytic and
265   For both vaccine regimens, natural killer (NK) cell signatures negatively correlated with and predi
266                     After ablation of mature NK cells, starting from day 15 after HSCT and favored by
267                     Classically, the CD56dim NK cell subset is thought to mediate antitumor responses
268                           Interestingly, the NK cell subsets that are more mature and possess higher
269  investigate clonal relationships of various NK-cell subsets, including the adaptive population, by t
270  via the AKT signaling pathway and increased NK cell survival and effector function.
271 seful for preclinical testing of novel human NK cell-targeted and combinatory cancer immunotherapies
272 nce may promote the design of individualized NK cell-targeted therapies to limit vascular damage in h
273 cquisition of cell migration as a feature of NK cell terminal maturation in this system.
274                                    Moreover, NK cells that expressed this mutant Ly49A exhibited an a
275  We observed a lower percentage of activated NK cells that produced less IFN-gamma upon coculture wit
276 rp1g is selectively expressed by a subset of NK cells, thereby potentially allowing for an inhibitory
277                          We stimulated human NK cells through CD16a in vitro, characterized CD16a-ind
278 lation restored reactivity of hyporesponsive NK cells through mTOR activation.
279 rs (BiKEs) which can bind to natural killer (NK) cells through the activating receptor CD16A and guid
280  innate lymphoid cells, and the capacity for NK cells to adapt and differentiate into long-lived memo
281                   Self-MHC-I also "licenses" NK cells to become responsive to activating stimuli and
282 uggest that the capability of HLA-C-licensed NK cells to control HIV-1 replication is determined by t
283 d to polarize the cytotoxic machinery of the NK cell toward the target cell.
284  T-cell clones were often observed in T- and NK-cell tumors in a percentage higher than observed in r
285                  Our data suggest that mouse NK cells use different signaling mechanisms for cytotoxi
286 n of Cy, a marked reduction of proliferating NK cells was evident, suggesting selective purging of di
287                    CD70 reverse signaling in NK cells was mediated via the AKT signaling pathway and
288                                Nevertheless, NK cells were able to sense alterations of HLA-C express
289                                              NK cells were infused on days -2, +7, and +28 posttransp
290                                              NK cells were responsible for such attenuated responses
291                   Canonical, PLZF-expressing NK cells were retained in asymptomatic carriers of GATA2
292 rmal levels of inflammatory monocytes, their NK cells were unresponsive to HSV-2 challenge.
293 he presence of CD4 T cells, CD8 T cells, and NK cells, where the loss of any one of these subsets led
294  ADCC is mediated largely by natural killer (NK) cells, which control their activation status through
295 known about their effects on natural killer (NK) cells, which help control metastasis.
296 26(-/-) mice have missing self-responses and NK cells with a normal receptor repertoire.
297 eraction between resting or stimulated human NK cells with M1 or M2.
298 ic avenues combing the killing efficiency of NK cells with the diversified target recognition of TCRs
299 CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49 recombinant chemokines using a singula
300 nd prolonged polarization toward neighboring NK cells without degranulation.

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