ライフサイエンスコーパス: killer cell

1 or) and lineage (B cell, T cell, and natural killer cell).

2 moral macrophages, and activation of natural killer cells.

3 ells enter into a differentiation process of killer cells.

4 which drives IFN-gamma production by natural killer cells.

5 cells, CD11c(+) dendritic cells and natural killer cells.

6 of each T-cell subset, B cells, and natural killer cells.

7 MHC-Ia molecules for presentation to natural killer cells.

8 osinophils, and enhanced circulating natural killer cells.

9 is produced by cytotoxic T cells and natural killer cells.

10 ding, fibroblasts to cytotoxicity by natural killer cells.

11 virus, and develop susceptibility to natural killer cells.

12 s of lymphomas arising from B, T, or natural killer cells.

13 tory signaling initiated by CD160 in natural killer cells.

14 lymphomas that arise from B, T, and natural killer cells.

15 onocytes, innate lymphoid cells, and natural killer cells.

16 was not able to stimulate T cells or natural killer cells.

17 nce of T cells, dendritic cells, and natural killer cells.

18 ctive cytotoxic T lymphocytes and/or natural killer cells.

19 to the shear stress and attack from natural killer cells.

20 monocytes, B cells, CD4 T cells, and natural killer cells.

21 d B cells and jak3 in T and putative Natural Killer cells.

22 rphic stress molecules recognized by natural killer cells.

23 lymphocytes because of a decrease in natural killer cells.

24 ly by regulatory T cells but also by natural killer cells.

25 t and the homologous FcgammaRIIIa on natural killer cells.

26 in controlling DENV infection using natural killer cells.

27 s well as decreased ICOS+ and 4-1BB+ natural killer cells.

28 xhibits SOX9-dependent resistance to natural killer cells.

29 "), especially cytotoxic T cells and natural killer cells.

30 ymphocyte attenuator (BTLA); and the natural killer cell-activating receptor CD160.

31 acute myeloid leukemia downregulate natural killer cell-activating receptor ligands to evade immune

32 ocytosis, cellular cytotoxicity, and natural killer cell activation were assessed.

33 on, IFNgamma response, CD16-mediated natural killer cell activation, and monocyte/macrophage activati

34 gocytosis, complement activation and natural killer cell activation, are substantially enhanced by a

35 Natural killer cell activities were clustered in clinical phases

36 L-12 and IL-15 in the enhancement of natural killer cell activity was reported.

37 cal defense, including inhibition of natural killer cell activity with ongoing lowering of Ig levels

38 ssion was an opportunity to discover natural killer cell alloreactions that eradicated acute myeloid

39 on profiles of a receptor protein in natural killer cells among donors infected with human cytomegalo

40 multiple human cell types, including natural killer cells, an IL-12 indicator cell line, and primary

41 lving phagosome formation as well as natural killer cell and IL-3 signaling.

42 an increased abundance of activated natural killer cells and a newly identified CD3(-)CD68(+)CD4(+)G

43 gnificantly decreased frequencies of natural killer cells and a trend toward reduced ILC populations,

44 ry cells, immunosuppressive CD56(hi) natural killer cells and ablation of proinflammatory mucosal-ass

45 pulations of myeloid cells, T cells, natural killer cells and B cells that demonstrated both pro-infl

46 Type I and II IFNs, as well as natural killer cells and CD8(+) T cells, were indispensible to t

47 Natural killer cells and cytotoxic T-lymphocytes deploy perforin

48 ncreased accumulation of T cells and natural killer cells and decreased myeloid-derived suppressor ce

49 ated with an increased proportion of natural killer cells and effector memory CD4(+) and CD8(+) T cel

50 a-induced pathways and activation of natural killer cells and endothelial cells.

51 ILCs consist of conventional natural killer cells and helper-like cells (ILC1, ILC2 and ILC3)

52 iency characterized by lack of T and natural killer cells and infant death from infection.

53 rs of IL-22 post-PH are conventional natural killer cells and innate lymphoid cells type 1.

54 s and dendritic cells) and lymphoid (natural killer cells and innate lymphoid cells) cell populations

55 ived PGE2 blocks early activation of natural killer cells and interferes with subsequent adaptive imm

56 ate lymphoid cells with conventional natural killer cells and lymphoid tissue inducer cells.

57 genous RNA editing enzyme in primary natural killer cells and lymphoma cell lines.

58 ly by suppressing IFNgamma-producing natural killer cells and M1-polarized macrophages.

59 wed exosomes were mainly taken up by natural killer cells and macrophages in the lung.

60 n HL cells and the CD16A receptor on natural killer cells and macrophages, to induce tumor cell killi

61 and binding to Fcgamma receptors on natural killer cells and macrophages.

62 ement deposition and accumulation of natural killer cells and monocytes/macrophages in capillaries an

63 ic macrophages, T and B lymphocytes, natural killer cells and platelets, as well as key effectors, su

64 receptors (KIRs) which are found on natural killer cells and some T cells; for the CD94:NKG2 family

65 Subsets of natural killer cells and T cells selectively induced nuclear fac

66 mpairing activation and functions of natural killer cells and T cells.

67 ral immune cell populations, such as natural killer cells and virus-specific T cells.

68 aRIIIa (expressed on macrophages and natural killer cells) and FcgammaRIIIb (expressed on neutrophils

69 totoxic cells (cytotoxic T cells and natural killer cells), and interleukin 12 production by antigen-

70 ed expression of IFNgamma-inducible, natural killer cell, and T cell transcripts, but less expression

71 ent-induced expansion of T cells and natural killer cells, and activation of interferon-gamma, T-cell

72 olled by T cells (T(H)1 and CD8(+)), natural killer cells, and antigen-presenting cells; T2 CRSsNP wa

73 tion of dendritic cells, mast cells, natural killer cells, and CD8 T cells to mount an antitumor immu

74 Teffs, natural killer cells, and eosinophils also responded, with their

75 e, including monocytes, neutrophils, natural killer cells, and eosinophils.

76 th correlated expression in T cells, natural killer cells, and erythroblasts.

77 T cells, reduced T-bet expression by natural killer cells, and expansion of blood monocytes with less

78 cking CD8 and CD4 T-cell activation, natural killer cells, and IFN activation associated significantl

79 ered in tropism, more susceptible to natural killer cells, and less pathogenic.

80 gamma and Granzyme B CD4 T cells and natural killer cells, and lower number of FoxP3 regulatory T cel

81 ght, including neutrophils, B cells, Natural Killer cells, and mast cells.

82 e the roles of alveolar macrophages, natural killer cells, and neutrophils in antibody-mediated prote

83 Tregs), gammadelta T cells, B cells, natural killer cells, and primary and induced pluripotent stem c

84 umor, activating dendritic cells and natural killer cells, and recruiting the adaptive immune system.

85 lar lavage samples and repression of natural killer cell- and T cell-associated transcripts in periph

86 + cytotoxic T lymphocytes (CTLs) and natural killer cells-and regulated by Runt-related (Runx) transc

87 Natural killer cells are able to directly lyse tumor cells, ther

88 T, B, and natural killer cells are required for normal immune response and

89 Cytotoxic T lymphocytes (T) and natural killer cells are the main cytotoxic killer cells of the

90 +) cytotoxic T lymphocytes (CTL) and natural killer cells are the main cytotoxic killer cells of the

91 yeloid-derived suppressor cells, and natural killer cells) as well as adaptive immune cells (T cells

92 immune cells (antitumor macrophages, natural killer cells) associated with clearance of senescent tum

93 still revealed diversity in a set of natural killer cell-associated receptors.

94 owed by MAIT, iNKT, gammadelta T and natural killer cells at the other end.

95 bacteria may not easily become resistant to killer cell attack.

96 a costimulatory receptor on T cells, natural killer cells, B cell subsets, and some dendritic cells.

97 e checkpoint receptors in T cell and natural killer cell biology are just beginning to be uncovered,

98 The killer cells bound to infected RBCs and killed intracell

99 inct lineage from Th and circulating natural killer cells but shares circuitry devoted to functional

100 suppress the cytotoxic functions of natural killer cells by a variety of mechanisms.

101 targets deployed in T cells (CAR-T), natural killer cells (CAR-NK) or mixtures (CAR-NK/T) from over 5

102 ting Kupffer cells, mature activated natural killer cells (CD69+), and PD-1+ effector memory T cells

103 mma-producing group 1 ILCs (ILC1 and natural killer cells), CD8(+) cytotoxic T cells (TC1), and CD4(+

104 mprised of two subsets, conventional natural killer cells (cNK) and tissue-resident cells often refer

105 uid (including B cells, T cells, and natural killer cells) (cohort 1).

106 bserved therapeutic effects and that natural killer cells constitute a critical human effector cell t

107 Natural killer cells constitute potent innate lymphoid cells tha

108 Natural killer cells controlled early infection but were not ess

109 onocytes, CD4(+) and CD8(+) T cells, natural killer cells, conventional and plasmacytoid dendritic ce

110 d with pretreatment levels, Treg and natural killer cell counts rose >fivefold (P < .001) and >fourfo

111 ell growth, including stimulation of natural killer cell cytotoxic activity and repression of Hedgeho

112 Natural killer cell deficiencies (NKDs) are an emerging phenotyp

113 Human natural killer cell deficiency (NKD) arises from inborn errors o

114 on (RTEL1) mutation causing isolated natural killer cell deficiency and mutations in ras-associated R

115 Specific natural killer cell depletion 24 hours pre-acute myocardial infa

116 aint in macrometastases triggered by natural killer cell depletion suggests a dynamic interplay betwe

117 1 cells than F1 cells was reduced by natural killer-cell depletion.

118 Natural killer cell development and maturation were arrested.

119 phenotype with a T-cell, B-cell, and natural killer cell developmental defect and hypogammaglobulinem

120 2DS1) expressed by maternal decidual natural killer cells (dNK) and the presence of its ligand, the H

121 -G+ EVT with sample matched decidual natural killer cells (dNK), macrophages, and CD4+ and CD8+ T cel

122 rt new mechanisms of human and mouse natural killer cell education by inhibitory and activating recep

123 pond to vaccines, there were reduced natural killer cells, elevated regulatory T cells, M2-type macro

124 Natural killer cells employ a diverse arsenal of effector mechan

125 cells (CAR-NKs), bispecific and trispecific killer cell engagers (BiKEs and TriKEs), checkpoint bloc

126 Bispecific killer cells engagers (BiKEs) which can bind to natural

127 The antibody-induced killer cells express, Granzyme B and Perforin that assau

128 Natural killer cells from acute myeloid leukaemia patients (AML-

129 or (TPOR) that effectively induces cytotoxic killer cells from precursor tumor cells isolated from ne

130 ules that seek to subvert T cell and natural killer cell function via a remarkable array of mechanism

131 at RAG endonuclease activity affects natural killer cell function, demonstrating that such double str

132 inflammation, T(H)17 signaling, and natural killer cell function.

133 Here, we show that natural killer cell granule protein 7 (NKG7) is a regulator of l

134 Killer-cell granzyme B also activates caspase-independen

135 ment induced TSLP, HLA class II, and natural killer cell group 2D (NKG2D) ligand expression in the le

136 Immunologically, natural killer cells had an immature phenotype and impaired cyto

137 tumor-specific cytotoxic T cells and natural killer cells, have been clinically translated for hemato

138 plied to other immune cells, such as natural killer cells, hematopoietic cells or induced pluripotent

139 The functions of activating members of the killer cell Ig-like receptor (KIR) family are not fully

140 Genetic case-control studies have implicated killer cell Ig-like receptor (KIR) genes and their HLA l

141 k showed that signaling by an HLA-C-specific killer cell Ig-like receptor (KIR) is independent of sig

142 The combination of the activating killer cell Ig-like receptor 2DS1 (KIR2DS1) expressed by

143 Human intrahepatic CD49a(+) NK cells express killer cell Ig-like receptor and NKG2C, indicative of ha

144 ptor genes encoded within the NK complex and killer cell Ig-like receptor genes encoded within the le

145 We proposed that the killer cell Ig-like receptor KIR3DL2 binding more strong

146 e gene diversity have focused on the MHC and killer cell Ig-like receptor.

147 ypes have the C1-epitope motif recognized by killer cell Ig-like receptor.

148 the differentiation stage, independently of killer cell Ig-like receptor/HLA class I-mediated inhibi

149 ceptors by their specific ligands, including killer cell Ig-like receptors (KIR) by classical MHC-I-p

150 The killer cell Ig-like receptors (KIR) modulate immune resp

151 with C1-specific and C2-specific lineage III killer cell Ig-like receptors (KIR).

152 Killer cell Ig-like receptors (KIRs) bind cognate HLA cl

153 Human NK cells carry inhibitory killer cell Ig-like receptors (KIRs), which recognize di

154 the inhibitory input by HLA class I-specific killer cell Ig-like receptors and CD94/NKG2A as well as

155 lotypes having the Bw4 epitope recognized by killer cell Ig-like receptors of NK cells, allotypes hav

156 the early markers c-kit and IL-7Ralpha, nor killer cell Ig-like receptors or other late-differentiat

157 pes having the C1 epitope also recognized by killer cell Ig-like receptors, and allotypes having neit

158 NK cells expressing self-specific inhibitory killer cell Ig-like receptors.

159 Killer cell immunoglobulin like receptors (KIRs) are a f

160 cognition of these HLA-B57 allomorphs by the killer cell immunoglobulin-like receptor (KIR) 3DL1 was

161 single locus in the centromeric motif of the killer cell immunoglobulin-like receptor (KIR) gene fami

162 uch as the human leukocyte antigen (HLA) and killer cell immunoglobulin-like receptor (KIR) regions.

163 ize, that NK cell alloreactivity mediated by killer cell immunoglobulin-like receptor (KIR)-HLA inter

164 in immunity, but how HLA class I (HLA-I) and killer cell immunoglobulin-like receptor 3DL1 (KIR3DL1)

165 upregulated NKp44 expression, and remarkable killer cell immunoglobulin-like receptor acquisition.

166 city, whereas knockdown of its receptor, the killer cell immunoglobulin-like receptor KIR3DL2, on hum

167 ells expressing self-MHC specific inhibitory killer cell immunoglobulin-like receptors (KIR) accumula

168 The inhibitory function of killer cell immunoglobulin-like receptors (KIR) that bin

169 gulate immune functions and are modulated by killer cell immunoglobulin-like receptors (KIR).

170 ion depend upon diverse interactions between killer cell immunoglobulin-like receptors (KIRs) and the

171 killer (NK) cell reactivity mediated through killer cell immunoglobulin-like receptors (KIRs) could r

172 ward infected or tumor cells is regulated by killer cell immunoglobulin-like receptors (KIRs) that bi

173 s diversity on the nanoscale organization of killer cell immunoglobulin-like receptors (KIRs).

174 ype, and more frequently expressed educating killer cell immunoglobulin-like receptors compared with

175 ith those utilized by T-cell receptor (TCR), killer-cell immunoglobulin-like receptor (KIR) and CD8 o

176 maternal natural killer (NK) cells that use killer-cell immunoglobulin-like receptor (KIR) to recogn

177 cyte immunoglobulin-like receptor (LILR) and killer-cell immunoglobulin-like receptor (KIR).

178 NK effector function depends on specific killer-cell immunoglobulin-like receptors (KIR) and HLA

179 ype is partially mediated through binding of killer-cell immunoglobulin-like receptors (KIR) with HLA

180 n contrast, dNK1 express receptors including Killer-cell Immunoglobulin-like Receptors (KIR), indicat

181 ) related to human leukocyte antigens (HLA), killer-cell immunoglobulin-like receptors (KIR), major h

182 her two major families of NK cell receptors, killer-cell immunoglobulin-like receptors (KIRs) and nat

183 wo highly polymorphic sets of molecules: the killer-cell immunoglobulin-like receptors (KIRs) and the

184 Additionally, these NKG2C NK cells expressed killer-cell immunoglobulin-like receptors distinct from

185 an increased ratio of neutrophils to natural killer cells in esophageal tissues compared with mice fe

186 l effects on B and T lymphocytes and natural killer cells in humans.

187 ells, and CD8 T lymphocytes and CD57 natural killer cells in the ALNs(-) were factors associated with

188 o extensive upregulation of APCs and natural killer cells in the blood and tumor compared with contro

189 MSCs significantly decreased natural killer cells in the heart and spleen and neutrophils in

190 ls via recruitment and activation of natural killer cells in the tumor.

191 Although the role of T cells and natural killer cells in tumor immunology has been established, l

192 ng normal numbers of CD8 T cells and natural killer cells in tumors.

193 es, monocytes, T cells, B cells, and natural killer cells) in patients having undergone HSPC gene the

194 NKG2A subset of CD56 natural killer cells increased substantially and persisted follo

195 grammed death ligand 1 expression on natural killer cells (increased from 11.9% to 61.6%, P = .03).

196 macrophages, innate lymphoid cells, natural killer cells, innate gammadelta T cells, and other signa

197 cytes, neutrophils, dendritic cells, natural killer cells, innate lymphoid cells-2, and CD (cluster o

198 lity of this microfluidic assay with natural killer cells interacting with tumor cells, and our findi

199 s, dendritic cells, macrophages, and natural killer cells is crucial for its protection.

200 tudy to ascertain the association of natural killer cell killer immunoglobulin-like receptors and hum

201 long with CRISPR/Cas9-KO cell lines, natural killer cell-killing assays, and RNA-Seq experiments, we

202 adults; for example, increased expression of killer cell lectin-like receptor B1 (KLRB1; CD161) 28 da

203 Further, we examined killer cell lectin-like receptor G1 (KLRG1) as a marker

204 cells with high expression of the inhibitory killer cell lectin-like receptor G1 (KLRG1) in individua

205 nt CD4+ and CD8+ T cells expressing CD57 and killer cell lectin-like receptor G1 (KLRG1), which was n

206 Reduced numbers of ADAP-deficient killer cell lectin-like receptor G1(-) CD8 resident memo

207 was a statistically significant reduction in killer cell lectin-like receptor mRNA expression between

208 nal differentiation including an increase in killer cell lectin-like receptor subfamily G member 1 an

209 s away from an APC-like phenotype and toward killer cell-like functions.

210 The function of natural killer cells, lymphocyte phenotype, and serum immunoglob

211 une cells including the conventional natural killer cells, lymphoid tissue inducers, type 1, 2, and 3

212 site-specific C-to-U RNA editing in natural killer cells, lymphoma cell lines, and, to a lesser exte

213 cells such as primary T and B cells, natural killer cells, macrophages, and primary microglia.

214 nosine signaling is found to promote natural killer cell maturation and antitumor immunity and reduce

215 ontext, supporting the hypothesis of natural killer cell mechanosensitivity.

216 at CD8 T cells, but not CD4 cells or natural killer cells, mediated elimination of KPC-Par-1(KO) tumo

217 e, pointing to the potential role of natural killer cell-mediated antibody-dependent cell cytotoxicit

218 ti-CD47 mAb induced phagocytosis and natural killer cell-mediated cytotoxicity of TCL cells that was

219 domain attenuated Necl-5 binding and natural killer cell-mediated cytotoxicity.

220 thout IL-5 was only seen in EOs, and natural killer cell-mediated eosinophil killing was seen only wi

221 Killer cell-mediated parasite death, which we term 'micr

222 hanisms important to generate innate natural killer cell "memory" are poorly understood.

223 Our results suggest that natural killer cells modified with glycan ligands to CD22 and se

224 + T cells, CD56 + T cells, CD56(dim) natural killer cells, monocytes and dendritic cells were not red

225 ng cytotoxic effector cells, such as natural killer cells, monocytes, and polymorphonuclear cells.

226 body can induce even relapsed AML cells into killer cells more potently than newly diagnosed AML cell

227 cule Stimulator of Interferon Genes, natural killer cells, myeloid cells, and B cells.

228 ns, including innate lymphoid cells, natural killer cells, natural killer T cells, mucosal-associated

229 patic macrophage infiltration, while natural killer cells, natural killer T cells, neutrophils and de

230 on of innate immunity in infants and natural killer cell networks in children, and additionally demon

231 regulatory T cells, dendritic cells, Natural Killer cells, neutrophils, and mast cells are present in

232 ivating or inhibitory effects during natural killer cell (NK cell) activation.

233 u modify the tumor cell surface with natural killer cell (NK cell)-activating signals to achieve in s

234 A tissue-resident population of natural killer cells (NK cells) in the liver has recently been d

235 Natural killer cells (NK) are highly enriched in the human liver

236 ratio and increased CD16(+)CD56(hi) natural killer cells (NK), CD4(+) effector memory T cells (Tem),

237 eloid DCs; neutrophils; macrophages; natural killer cells (NK); Marginal Zone-like B cells (MZB); gam

238 mory CD8(+) T cells (TRMs), resident natural killer cells (NKRs), and tumor-associated macrophages (T

239 Natural killer cells (NKs) are important effectors of the innate

240 Cytotoxic T-lymphocytes (CTLs) and natural killer cells (NKs) kill compromised cells to defend agai

241 absent T cells and normal B-cell and natural killer cell numbers.

242 timulated both cytotoxic T cells and natural killer cells of cell-mediated immunity to provide tumor

243 natural killer cells are the main cytotoxic killer cells of the human body to eliminate pathogen-inf

244 natural killer cells are the main cytotoxic killer cells of the human body to eliminate pathogen-inf

245 ite replication, possibly as innate parasite killer cells or function in eliciting pathogenesis.

246 In contrast to viral evasion of natural killer cells or T cell recognition, the evasion of antib

247 Furthermore, a shift in the natural killer cell phenotype was observed with features suggest

248 Natural killer cells play an important role in immunity to many

249 er, CD8+ T-cell, CD4+ T-cell and NK (natural killer) cell populations in splenocytes were elevated in

250 A combination of serum and natural killer cells provided the most effective protection agai

251 requencies of intrathecal CD56bright natural killer cells (r = 0.28; P = .007).

252 Natural killer cells readily kill target cells, and education en

253 3-like ILCs was not dependent on the natural killer cell receptor (NCR1), since NCR1-deficient mice s

254 Killer cell receptor genes encoded within the NK complex

255 Natural killer cell receptors and other genes related to the imm

256 forming ligands for cytotoxic T and natural killer cell receptors.

257 complexes probably affect T-cell and natural killer cell recognition, providing a sound basis for the

258 are due to a different proportion of natural killer cells responding in LUJV infection than that in t

259 h CMVs evade or reprogram T cell and natural killer cell responses in vivo However, the role of humor

260 137 MAb that can activate T cell and natural killer cell responses to clear tumors.

261 Simultaneously, natural killer cell responses to inflammatory cytokines were att

262 y pathology, stronger and persistent natural killer cell responses, and the extended induction of pro

263 to local and systemic recruitment of natural killer cells resulting in increased interferon-gamma exp

264 By contrast, natural killer cells retained partial IL-2Rbeta expression and f

265 The mechanisms underlying killer cell's navigation are not well understood.

266 ry and regulatory cytokine profiles, natural killer cells showed a predominantly proinflammatory prof

267 Natural killer cells showed reduced T-bet expression at day 1 wi

268 oupled with T-helper cell type 2 and natural killer cell signaling in children.

269 ith an additional role of T(H)17 and natural killer cell signaling.

270 r of tumor-infiltrating CD8(+) T and natural killer cells, slowed tumor growth, and improved mouse su

271 Quantification of natural killer cells spreading on surfaces coated with the nanob

272 RNA-seq analysis of natural killer cells subjected to cellular crowding and hypoxia

273 Natural killer cell subset association with CMV endpoints were m

274 he death of CD56(bright) NK cells, a natural killer cell subset whose expansion is correlated with au

275 composition of gammadelta T-cell and natural killer cell subsets.

276 okine milieu, macrophages/monocytes, natural killer cells, T cells, and neutrophils in severe COVID-1

277 matory cytokine responses by DCs and natural killer cells, Th1 development, phagocytic receptor expre

278 -producing dendritic cells (DCs) and natural killer cells than Cd36(-/-) mice.

279 lly changing channel network produced by the killer cells themselves.

280 ds onto NK-92MI and cytokine-induced natural killer cells to achieve tumor-specific CD22 targeting.

281 anced the activity and maturation of natural killer cells to effectively treat anti-PD-1 resistant tu

282 2B8T2M activates natural killer cells to enhance antibody-dependent cellular cyto

283 reted by cytotoxic T lymphocytes and natural killer cells to help eliminate virus-infected and transf

284 at anti-CD27 stimulated CD8(+) T and natural killer cells to release myeloid chemo-attractants and in

285 e cells, such as T helper type 1 and natural killer cells, to unleash neurotoxicity and inflammation-

286 inical investigation of lymphokine-activated killer cells, tumour-infiltrating lymphocytes, and allog

287 Because killer cells use a multipronged strategy to target vital

288 Additionally, NKG7 expressed by natural killer cells was critical for controlling cancer initiat

289 IFN-gamma production, mainly by natural killer cells, was associated with protection, and a posi

290 ession on CD8(+) T cells, but not on natural killer cells, was required for optimal anti-ErbB2 mAb ef

291 stocompatibility complex class I and natural killer cells were commonly downregulated in psoriasis an

292 Moreover, natural killer cells were involved in AS by increasing the acces

293 Natural killer cells were normal in number but not "licensed to

294 Specifically, T, B, and natural killer cells were severely depleted in the blood by day

295 n by IL-12p70-mediated activation of natural killer cells, whereas miR-146a and miR-146b overexpressi

296 n in NKG2A and NKG2C subsets of CD56 natural killer cells which might have a pathogenic role in chron

297 grafts is driven by the recipient's natural killer cells, which overwhelmingly use perforin to kill

298 infection, for example proliferating natural killer cells, which potentially may associate with futur

299 tively recruited and activated human natural killer cells, while vaccine-elicited RM antibodies were

300 y disease (SCID) affecting B, T, and natural killer cells, with an almost complete lack of antibodies