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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
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
39 objective was to determine the difference in NK cell activity between subjects with vs without CRC.
42 oscopy as the reference standard, a test for NK cell activity in whole blood samples identified patie
45 y of infusing high doses of ex vivo-expanded NK cells after haploidentical HSCT without adverse effec
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
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
57 l death and survival pathways and implicated NK cells and neutrophil populations in this differential
59 vo restored perforin expression in CD56(dim) NK cells and partially restored NK cell cytotoxic functi
62 sion in Ifitm3-/- mice triggered the loss of NK cells and subsequently impaired control of MCMV repli
64 he former treatment activates nature killer (NK) cells and NK T cells, which partially enhances the i
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
71 these studies indicate that tissue-resident NK cells are evolutionarily conserved in humans and mice
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
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
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
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
100 gene turnover of trans-membrane proteins in NK cells compared with T cells in fish species, suggesti
103 t induce the Zap70(low)Syk(low) phenotype in NK cells: continuous stimulation with activation beads a
105 sceptibility of cisplatin-resistant cells to NK cell cytotoxicity when neutralizing antibody of PD-1
111 gnature of genes present in mouse ILC except NK cells, defined by Immunological Genome Project studie
116 we show that STAT5 dimers are sufficient for NK cell development, whereas STAT5 tetramers mediate NK
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
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).
129 virus (MCMV)-encoded protein, m12, restrains NK cell effector function by directly engaging the inhib
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
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
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
144 lation with target cells, Zap70(low)Syk(low) NK cells failed to produce IFN-gamma and lysed target ce
146 hus, during GVHD, donor T cells compete with NK cells for IL-15 thereby inducing profound defects in
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
154 or genetic ablation of innervation preserved NK cell function and restrained post-stroke infection.
157 ctivation is crucial in regulating pulmonary NK cell function, and suggest that NK cells serve to lim
160 itabine (DAC) in combination with allogeneic NK cells generated from CD34(+) hematopoietic stem and p
163 te-of-the-art mouse models, demonstrate that NK cells have no direct effect on the natural developmen
168 ver, mice lacking heparanase specifically in NK cells (Hpsefl/fl NKp46-iCre mice) were highly tumor p
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
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
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.
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
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
194 bound interleukin 21 (mbIL21) expanded donor NK cells infused before and after haploidentical HSCT fo
196 numbers, whereas transfer of CD3(-)NK1.1(+) NK cells into the airways of WT hosts suppressed the inf
200 of normal articular chondrocytes to lysis by NK cells is modulated by NKR-P1A/LLT1 interactions.
202 lymphoid cells (ILC1s) from natural killer (NK) cells is a gene signature indicative of 'imprinting'
205 acking classical B-, T-, and natural killer (NK)-cell lineage markers (Lin(-)IELs) in the duodenum.
207 emokine receptor CXCR4 were all required for NK cell localization during homeostasis and rapid produc
213 development, whereas STAT5 tetramers mediate NK cell maturation and the expression of maturation-asso
215 n, expansion, and adoptive transfer of these NK cells may allow monitoring of treatment efficacy and
217 s targeting the V1V2 domain induce up to 60% NK cell mediated lysis of HIV-1 infected PBMCs in a phys
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
223 d was associated with significantly improved NK-cell number and function, lower viral infections, and
225 leads to splenic atrophy and contraction of NK cell numbers in the periphery through a modulated exp
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
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
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
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
244 peptide-dependent binding of the activating NK cell receptor KIR2DS1, providing new insights into th
247 r IL-15 thereby inducing profound defects in NK-cell reconstitution that compromise both leukemia and
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
256 Notably, A2AR-deficient, terminally mature NK cells retained proliferative capacity and exhibited h
261 pulmonary NK cell function, and suggest that NK cells serve to limit ILC2 activation and subsequent a
263 D mice, which have a deficiency in T, B, and NK cells, showed minimal disease at cutaneous sites but
265 For both vaccine regimens, natural killer (NK) cell signatures negatively correlated with and predi
269 investigate clonal relationships of various NK-cell subsets, including the adaptive population, by t
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
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
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
282 uggest that the capability of HLA-C-licensed NK cells to control HIV-1 replication is determined by t
284 T-cell clones were often observed in T- and NK-cell tumors in a percentage higher than observed in r
286 n of Cy, a marked reduction of proliferating NK cells was evident, suggesting selective purging of di
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
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
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