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 elper T cells, effector B cells, and natural killer cells).

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

4 lymphocytes because of a decrease in natural killer cells.

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

6 nsitizing melanoma cells to lysis by natural killer cells.

7 s in CD4+ T cells, CD8+ T cells, and natural killer cells.

8 und to be less sensitive to purified natural killer cells.

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

10 red for the development of classical natural killer cells.

11 l dendritic cells, and activation of natural killer cells.

12 iral immune responses of T cells and natural killer cells.

13 e in the development and activity of natural killer cells.

14 nules of cytotoxic T lymphocytes and natural killer cells.

15 by both antigen-specific T cells and natural killer cells.

16 bound H1 hemagglutinin and activated natural killer cells.

17 n by antibody-dependent clearance by natural killer cells.

18 ding, fibroblasts to cytotoxicity by natural killer cells.

19 ably monocytes, dendritic cells, and natural killer cells.

20 monocytes/macrophages, T cells, and natural killer cells.

21 n turn enhances tumor elimination by natural killer cells.

22 virus, and develop susceptibility to natural killer cells.

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

24 tory signaling initiated by CD160 in natural killer cells.

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

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

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

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

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

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

31 Splenic natural killer cells activated upon Pseudomonas aeruginosa infec

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

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

34 and chemokine levels, lymphocyte and natural killer cell activation, and viral antigen expression.

35 1 ECs enhanced NKG2D interaction and natural killer cell activation, promoting NKG2D-dependent lysis

36 Natural killer cell activities were clustered in clinical phases

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

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

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

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

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

42 hesion molecule, expressed mainly by natural killer cells and CD8(+) T cells at steady state to promo

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

44 Natural killer cells and cytotoxic T-lymphocytes deploy perforin

45 reduce the viability of normal T and natural killer cells and decrease activated T-cell production of

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

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

48 reduced this suppressive function of natural killer cells and increased survival of mice with posthem

49 ce, mimics the cytotoxic activity of natural killer cells and increases the surface area available fo

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

51 Natural killer cells and injured grafts may play a reciprocal ro

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

53 After INT-747 treatment, natural killer cells and interferon-gamma expression markedly de

54 -/-) mice, but perforin induction by natural killer cells and levels of interferon gamma, interleukin

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

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

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

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

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

60 -17 production by CD4(+) T cells and natural killer cells and recruited regulatory cells and neutroph

61 I) ligands and regulate functions of natural killer cells and subsets of T cells.

62 76) is both an inhibitory ligand for natural killer cells and T cells and a tumor antigen that is wid

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

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

65 ent elimination of dendritic cell by natural killer cells and that hydrocortisone improves outcome by

66 ent of innate lymphocytes, including natural killer cells and the recently identified innate lymphoid

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

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

71 immune cells, including neutrophils, natural killer cells, and B cells.

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

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

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

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

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

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

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

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

80 tivated interferon-stimulated genes, natural killer cells, and lymphocyte subsets.

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

82 acrophages, myeloid dendritic cells, natural killer cells, and T cells in SCC vs normal skin.

83 Natural killer cells are a type of cytotoxic lymphocyte and part

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

85 Natural killer cells are innate lymphocytes that play vital role

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

87 Neutrophils and natural killer cells are the likely targets of these pathways, b

88 effective in ADCC assays with murine natural killer cells as effectors, whereas ADCP was equivalent f

89 Natural killer cells assess target cell health via interactions

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

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

92 and alternate macrophage, B-cell and natural killer cell-associated transcripts (NKAT), indicating an

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

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

95 ithin antigen-experienced T cells or natural killer cells but less so in naive T or B cells.

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

97 gly, tumor rejection did not involve natural killer cells but was associated instead with a marked in

98 ction of the interleukin-10 level in natural killer cells by hydrocortisone was partially dependent o

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

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

101 in the regulation of dendritic cell/natural killer cell cluster.

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

103 precursor, immature, and mature types), and killer cells (consisting of cytotoxic T cells, helper T

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

105 Natural killer cells constitute potent innate lymphoid cells tha

106 Natural killer cells controlled early infection but were not ess

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

108 rtisone modulates the dendritic cell/natural killer cell cross talk in the context of posttraumatic p

109 of hydrocortisone on dendritic cell/natural killer cell cross talk were studied in a mouse model of

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

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

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

113 Natural killer cell depletion or codepletion of CD4(+) and CD8(+

114 In contrast, decidual natural killer cell-derived IFN-gamma reverses such TNF-alpha-in

115 Natural killer cell development and maturation were arrested.

116 Ultimately, mice depleted of natural killer cells displayed an increased neutrophil numbers i

117 interaction of noncytotoxic decidual natural killer cells (dNK) and extravillous trophoblasts (EVT) a

118 2DS1) expressed by maternal decidual natural killer cells (dNK) and the presence of its ligand, the H

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

120 molecules) were increased in splenic natural killer cells during Pseudomonas aeruginosa infection.

121 ell effector functions, and variable natural killer cell dysfunctions.

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

123 marrow MDS-NK cells treated with bispecific killer cell engager (BiKE) significantly enhanced degran

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

125 Natural killer cells express multiple receptors for major histoc

126 Cytotoxic T lymphocytes and natural killer cells expressing granulysin predominantly infiltr

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

128 Natural killer cell function is regulated by inhibitory and acti

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

130 oteins, many of which interfere with natural killer cell function.

131 lymphocytes and T-regulatory cells, natural killer cells, gamma delta T cells, and other accessory c

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

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

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

135 The resulting "unnatural killer cells" hold promise as an effective means to neut

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

137 KIR2DL4 (CD158d) is a distinct member of the killer cell Ig-like receptor (KIR) family in human NK ce

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

139 ns are linked to combinations of polymorphic killer cell Ig-like receptor (KIR) genes expressed by ma

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

141 The human killer cell Ig-like receptor (KIR) locus comprises two g

142 T recipients or controls, is a population of killer cell Ig-like receptor (KIR)-expressing CD8 T cell

143 The endosomal innate receptor CD158d (killer cell Ig-like receptor 2DL4) induces cellular sene

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

145 The killer cell Ig-like receptor 3DL1 (KIR3DL1) inhibits act

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

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

148 TLR and TNFR signaling pathway is used by a killer cell Ig-like receptor that promotes secretion of

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

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

151 KG2A operates in tandem with the polymorphic killer cell Ig-like receptors (KIR) and Ly49 systems to

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

153 ells by virtue of inhibitory NKRs, primarily killer cell Ig-like receptors (KIR) that bind "self" HLA

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

155 specific receptors, including the inhibitory killer cell Ig-like receptors (KIRs) and the lectin-like

156 Inhibitory killer cell Ig-like receptors (KIRs) are known to recogn

157 Unexpectedly, diversified killer cell Ig-like receptors (KIRs) are shared by simia

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

159 Peptide:MHC complexes that bind weakly to killer cell Ig-like receptors (KIRs) can antagonize the

160 Killer cell Ig-like receptors (KIRs) interact with HLA c

161 table surface expression of human inhibitory killer cell Ig-like receptors (KIRs) is critical for con

162 on of MHC class I ligands for rhesus macaque killer cell Ig-like receptors (KIRs) is fundamental to o

163 Killer cell Ig-like receptors (KIRs) on NK cells have be

164 iated by NK cells is regulated by inhibitory killer cell Ig-like receptors (KIRs), which interact wit

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

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

167 - and nonself-HLA class I-binding inhibitory killer cell Ig-like receptors contributed, to a similar

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

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

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

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

172 feron-gamma (IFN-gamma) by activated natural killer cells, IL-34-Mphi and M-CSF-Mphi prevent the IFN-

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

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

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

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

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

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

179 CSF2); interferon gamma receptor 2 (IFNGR2); killer cell immunoglobulin-like receptor, three domain,

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

181 on is regulated by inhibitory and activating killer cell immunoglobulin-like receptors (KIR).

182 ibility complex (MHC) class I, including the killer cell immunoglobulin-like receptors (KIRs) and the

183 ler (NK) cells are functionally regulated by killer cell immunoglobulin-like receptors (KIRs) and the

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

185 Killer cell immunoglobulin-like receptors (KIRs) play an

186 human immunity and reproduction are diverse killer cell immunoglobulin-like receptors (KIRs) that re

187 The engagement of natural killer cell immunoglobulin-like receptors (KIRs) with th

188 ins by diverse receptor families such as the killer cell immunoglobulin-like receptors (KIRs), and (i

189 Killer cell immunoglobulin-like receptors (KIRs), via in

190 y interest are a group of genes encoding the killer cell immunoglobulin-like receptors (KIRs), which

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

192 We analyzed the influence of donor killer-cell immunoglobulin-like receptor (KIR) gene hapl

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

194 Here, using a killer-cell immunoglobulin-like receptor (KIR) transgeni

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

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

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

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

199 Because activating killer cell immunoglobulinlike receptors (KIRs) are hete

200 We assessed the role of systemic natural killer cells in a Pseudomonas aeruginosa mouse pneumonia

201 ineered HSCs may produce myeloid and natural killer cells in addition to T cells expressing the CAR,

202 ed activity of cytotoxic T cells and natural killer cells in BKVN and viremia samples resembling acut

203 The percentage of natural killer cells in granulomas was significantly decreased i

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

205 ates IFNgamma release in T cells and natural killer cells in response to interleukin 12 (IL12).

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

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

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

209 e-induced immunosuppression, splenic natural killer cells induced an interleukin-10-dependent elimina

210 e balance of signals received by the natural killer cell influences its involvement in the ensuing im

211 ate lymphocytes (gammadelta T cells, natural killer cells, innate lymphoid cells) are the major sourc

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

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

214 irement of the T cell differentiation marker killer cell lectin-like receptor G1 (KLRG1) during M. tu

215 (+) T cells had decreased CD27 and increased killer cell lectin-like receptor G1 (KLRG1) expression.

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

217 generate a robust terminally differentiated killer cell lectin-like receptor G1 (KLRG1)(hi) effector

218 of interleukin-7 receptor and low levels of killer cell lectin-like receptor G1 [IL-7Rhi KLRG1lo]) a

219 This led to generation of CD8(+)/killer cell lectin-like receptor G1 high (KLRG1(hi))/IL-

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

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

222 sion and function of an inhibitory receptor, killer cell lectin-like receptor subfamily G member 1 (K

223 nd increased expression of NKG2D (CD314) and killer cell lectin-like receptor subfamily G member 1 (K

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

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

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

227 9 (TLR9), induces the activation of natural killer cells, macrophages, and antigen presenting cells

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

229 G1 was evaluated in vitro by using a natural killer cell-mediated killing assay and in vivo in cynomo

230 anti-EMR1 mAb dramatically enhanced natural killer cell-mediated killing of eosinophils from healthy

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

232 t mitophagy plays a critical role in natural killer cell memory formation following viral infection.

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

234 her leukocyte populations, including natural killer cells, monocytes, and dendritic cells, show alter

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

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

237 f T cells, B cells, dendritic cells, natural killer cells, myeloid-derived suppressor cells, neutroph

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

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

240 wed that parameters controlling the level of killer cell neutrophils affected the overall systemic da

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

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

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

244 Fluorescently labeled human T cells, natural killer cells (NK), and various target cells (NALM6, K562

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

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

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

248 Natural killer cell number and status were assessed in spleen (f

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

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

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

252 specific ADCC antibodies to activate natural killer cells (P<.001).

253 that innate immune factors, such as natural killer cells, plasmacytoid dendritic cells, and the expr

254 e alterations of dendritic cells and natural killer cells play a central role in trauma-induced immun

255 We report for the first time that natural killer cells play a major role in the mice susceptibilit

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

257 Thus killer cells play an unexpected role in bacterial defens

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

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

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

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

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

263 are Patr-B variants that engage with natural killer cell receptors.

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

265 tion, innate immune cells, including natural killer cells, recovered with virus rebound.

266 m the lung vasculature, and promoted natural killer cell recruitment and activation.

267 In this setting, the role of natural killer cells remains controversial.

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

269 sult from impaired CD8(+) T-cell and natural killer cell responses to EBV infection in these patients

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

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

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

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

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

275 f CD4+ FoxP3+ T cells and CD56(high) natural killer cell subsets, which are cell subsets associated w

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

277 ve shown major shifts in circulating natural killer cells, T and B lymphocytes immediately after stem

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

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

280 R3 and RLR to activate dendritic and natural killer cells that can kill tumor cells.

281 ing evidence for the contribution of natural killer cells, the key mediators of antibody-dependent ce

282 RAIL is part of the armamentarium of natural killer cells, these observations identify a new facet of

283 2B8T2M activates natural killer cells to enhance antibody-dependent cellular cyto

284 ndependent MET activity, and engaged natural killer cells to kill MET-expressing cancer cells, displa

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

286 icidal effector cells, in particular natural killer cells, to the tumor stroma for antitumor activity

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

288 Because killer cells use a multipronged strategy to target vital

289 Depletion of natural killer cells was achieved through an IV anti-asialo-GM1

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

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

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

293 dependent on CD8(+) T cells, whereas natural killer cells were dispensable.

294 gs, indicating that mice depleted of natural killer cells were much more susceptible to infection com

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

296 The blood levels of natural killer cells were not altered in brain-injured patients.

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

298 Blood CD16 and CD56 natural killer cells were significantly more likely to be elevat

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

300 mma) or TNF-alpha or cocultured with natural killer cells (which have been shown to induce anti-M. av