ライフサイエンスコーパス: T-lymphocyte

1 IS is essential for the development of B and T lymphocytes.

2 TING activation reduces the proliferation of T lymphocytes.

3 12-induced LFA-1 activation in human primary T lymphocytes.

4 enous STING inhibited proliferation of mouse T lymphocytes.

5 ce in the recruitment of macrophages or B or T lymphocytes.

6 number of hematopoietic lineages, including T lymphocytes.

7 load in the lungs and caused recruitment of T lymphocytes.

8 o the exometabolomic profile of fetal CD4(+) T lymphocytes.

9 from murine T helper type 17-differentiated T lymphocytes.

10 t ultimately elicit immune control by CD8(+) T lymphocytes.

11 lts in a decreased number of cytotoxic CD8(+)T lymphocytes.

12 l fibroblasts (SF) and local infiltration of T lymphocytes.

13 gous dendritic cells and even tumor-reactive T lymphocytes.

14 resulting in the generation of mature B and T lymphocytes.

15 liva induces the production of IL-10 by CD8+ T lymphocytes.

16 and Cxcl10, two potent chemoattractants for T lymphocytes.

17 t is normally eliminated by CD8(+) cytotoxic T lymphocytes.

18 f antigens by dendritic cells (DCs) to naive T lymphocytes.

19 erted roles on vascular cells, monocytes and T lymphocytes.

20 oles in the normal physiological function of T lymphocytes.

21 ulate gene expression and functions of human T lymphocytes.

22 onship between these innate immune cells and T lymphocytes.

23 oteins is a fundamental signaling pathway in T lymphocytes.

24 nduction in activated intraepithelial CD8(+) T lymphocytes.

25 it an immune response from CD4(+) and CD8(+) T lymphocytes.

26 (iNKT) cells, a specialized subset of innate T lymphocytes.

27 ritically dependent on central memory CD8(+) T lymphocytes.

28 l reduction in the number of tumor cytotoxic T lymphocytes.

29 he apex of the hierarchical system of memory T lymphocytes.

30 t a heterogeneous population of infiltrating T lymphocytes.

31 presenting immunogenic peptides to cytotoxic T lymphocytes.

32 frequencies of macrophages, neutrophils, and T lymphocytes.

33 controlled the fate specification of CD8(+) T lymphocytes.

34 controls the cytotoxicity of mouse cytotoxic T lymphocytes.

35 ophils and DCs and a concomitant decrease in T lymphocytes.

36 mited by the increase in alloreactive CD4(+) T lymphocytes.

37 ession of the activity of tumor-infiltrating T lymphocytes.

38 by cancer cells in response to the activated T-lymphocytes.

39 ate directional migration of neutrophils and T-lymphocytes.

40 ilver (Ag) in individual Ag NP exposed human T-lymphocytes.

41 ctivation were unique to HCA-positive CD4(+) T lymphocytes; 3) metabolic pathways associated with glu

42 y, yet transiently, decrease numbers of CD4+ T lymphocytes, a major reservoir for human immunodeficie

43 Depletion of CD4(+) or CD8(+) T lymphocytes abolished this growth inhibition, identify

44 Ag recognition induces T lymphocyte activation and proliferation and acquisitio

45 tion-induced suppression of cytotoxic CD8(+) T-lymphocyte activation as a tumour-promoting mechanism.

46 RLK, two Tec kinases activated downstream of T-lymphocyte activation, both of which are up-regulated

47 ATc1 binds many genes that control cytotoxic T lymphocyte activity.

48 ivity, we measured a significant decrease in T lymphocyte adhesion and consequently transmigration bo

49 GEF1, and DOCK2 impairs LFA-1-mediated rapid T lymphocyte adhesion as well as underflow arrest on ICA

50 timulation of integrin alpha4beta1-dependent T lymphocyte adhesion is a key step during lymphocyte tr

51 +)CD8(+) T cells and neoantigen-specific CD8 T lymphocytes against the marker neoepitope LAMA4-G1254V

52 T lymphocyte alterations are central to sepsis pathophys

53 ibited reduced kidney leukocyte recruitment (T lymphocytes and classic M1 proinflammatory macrophages

54 engineer human beta-cell-specific cytotoxic T lymphocytes and demonstrate that T1-IFN augments cytot

55 ted by antigen-specific interactions between T lymphocytes and dendritic cells (DCs).

56 5 days was prevented by depletion of CD8(+) T lymphocytes and did not require GM-CSF, as mpJX-594 va

57 f LAT to the immune synapse in naive primary T lymphocytes and for effective T-cell responses in vivo

58 central nervous system (CNS) recruitment of T lymphocytes and inflammatory myeloid cells, while peri

59 T lymphocytes and macrophages both display immunosuppres

60 vating type 1 angiotensin (AT1) receptors in T lymphocytes and myeloid cells blunts the polarization

61 IFNgamma-producing CD8(+) tumor-infiltrating T lymphocytes and results in a profound extension of the

62 critical for malignant transformation of the T lymphocytes and that progression of the disease is dep

63 of CD28 costimulation on established memory T lymphocytes and the recall of memory responses remain

64 signaling between antigen receptors on B and T lymphocytes and the transcription factor NF-kappaB dur

65 ing identified macrophages/microglia, CD4(+) T lymphocytes, and neutrophils in the glioma microenviro

66 including brain, purified neurons and glia, T lymphocytes, and placenta, and identify 795 hap-ASM di

67 radation were altered in HCA-positive CD4(+) T lymphocytes; and 4) flow cytometry and cytokine analys

68 mbination-mediated assembly of diverse B and T lymphocyte antigen receptor (AgR) genes is not only es

69 e evaluated Eomes and coinhibitory cytotoxic T lymphocyte antigen-4 (CTLA4) expression by alloactivat

70 programmed cell death 1 [PD-1] and cytotoxic T-lymphocyte antigen 4 [CTLA-4]) was similar to that of

71 Neutralization of cytotoxic T-lymphocyte antigen 4 and transforming growth factor-be

72 sponses, blocking antibodies (anti-cytotoxic T-lymphocyte antigen 4, anti-programmed death ligand 1)

73 xpression of regulatory molecules (cytotoxic T-lymphocyte antigen 4, programmed cell death 1, and ind

74 mor T-cell responses by binding to cytotoxic T-lymphocyte antigen 4.

75 rine tumor xenograft model of anti-cytotoxic T-lymphocyte antigen-4 (CTLA-4) immunotherapy of colon c

76 one or combined with ipilimumab (a cytotoxic T-lymphocyte antigen-4 checkpoint inhibitor), have not b

77 ssion, BRAF status, and best prior cytotoxic T-lymphocyte antigen-4 therapy response, then randomly a

78 with integrin signaling pathways to promote T-lymphocyte antitumor functions, with potential implica

79 ssive stress-induced steroids cause immature T-lymphocyte apoptosis in thymus.

80 show that antigen-specific B lymphocytes and T lymphocytes are activated in piperacillin-hypersensiti

81 Cytotoxic T lymphocytes are effector CD8(+) T cells that eradicate

82 IFN-gamma-producing cytotoxic T lymphocytes are essential for host defense against vir

83 CD4(+) T lymphocytes are globally expanded and activated in chr

84 zed, the metabolic demands of differentiated T lymphocytes are largely unexplored.

85 Vgamma9Vdelta2 T lymphocytes are the major human peripheral gammadelta

86 Absolute numbers of CD4 and CD8 T-lymphocytes are commonly reduced after brain death in

87 that NKT cells, a population of innate-like T lymphocytes, are critical for the induction of B cell

88 eases mediated by a type of white blood cell-T lymphocytes-are currently treated using mainly broad-s

89 st the preferential targeting of PEG-HCCs to T lymphocytes as a novel approach for T lymphocyte immun

90 man peripheral blood B, CD4(+) T, and CD8(+) T lymphocytes as well as switched memory B cells are mos

91 programmed cell death 1 (PD-1) and cytotoxic T-lymphocyte associated protein 4 (CTLA4), down-regulate

92 ression of the inhibitory molecule cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) on CD4(+) T c

93 ige-like anchor protein (LRBA) and cytotoxic T lymphocyte-associated antigen 4 (CTLA4) deficiencies g

94 demonstrate reduced expression of cytotoxic T lymphocyte-associated genes and IFN-gamma-inducible ch

95 oint inhibitory antibodies against cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and programme

96 ed death ligand 1 (PD-1/PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) restored anti

97 n (PD) 1-PD ligand 1/2 pathway and cytotoxic T lymphocyte-associated protein 4 are currently the most

98 s investigating the combination of cytotoxic T lymphocyte-associated protein 4 inhibitors and PD-1/PD

99 ammed cell death protein 1 or anti-cytotoxic T lymphocyte-associated protein 4 is currently unknown.

100 we investigated the effects of the cytotoxic-T-lymphocyte-associated antigen 4 (CTLA-4) monoclonal an

101 F or MEK) or an immune checkpoint (cytotoxic T-lymphocyte-associated antigen 4 [CTLA-4] or programmed

102 a monoclonal antibody that blocks cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) signalling, i

103 blockade using antibodies against cytotoxic-T-lymphocyte-associated protein 4 (CTLA4) or programmed

104 Cytotoxic T-lymphocyte-associated protein 4 (CTLA4), which interac

105 , which regulates the induction of cytotoxic T-lymphocyte-associated protein 4 (CTLA4).

106 Belatacept (cytotoxic T-lymphocyte-associated protein 4 Ig) is an emerging tre

107 l aOX40 (anti-CD134)/aCTLA-4 (anti-cytotoxic T-lymphocyte-associated protein 4) immunotherapy generat

108 erleukin-2, interleukin-7, CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), T-cell receptor, and

109 e autophagic machinery in DCs in a cytotoxic T-lymphocyte-associated protein 4-dependent (CTLA4-depen

110 treatment, with administration of cytotoxic T-lymphocyte-associated protein 4-Ig reducing disease sy

111 These data suggest that cytotoxic T-lymphocyte-associated protein 4-Ig should be evaluated

112 impede protective immunity through cytotoxic-T-lymphocyte-associated protein-4 (CTLA-4).

113 identified a subset of CD8(+)PD-1(+)FOXP3(+) T lymphocytes at the earliest phase of functional differ

114 he immunoglobulin inhibitory receptor, B and T lymphocyte attenuator (BTLA); and the natural killer c

115 mmune cells, with three distinct clusters of T lymphocytes, B lymphocytes and macrophages.

116 nally, the effect of SWCNTs on the number of T lymphocytes, B lymphocytes and monocytes within the PB

117 c stem cell transplantation (HSCT) cures the T-lymphocyte, B-lymphocyte, and natural killer (NK)-cell

118 HC class I molecule HLA-A2 produce cytotoxic T lymphocytes bearing T-cell receptors (TCRs) that recog

119 te to establishing a productive infection in T lymphocytes but fails to induce an innate immune respo

120 n of freshly isolated human peripheral blood T lymphocytes, but not neutrophils or B lymphocytes, in

121 erapeutic approaches have largely focused on T lymphocytes, but the innate arm of the immune system m

122 target proinflammatory cytokines produced by T lymphocytes, but the need for improved therapies persi

123 In addition, activation of CD4(+) T lymphocytes by immune checkpoint blockade increased ve

124 sustained the in vitro activation of Vgamma9 T lymphocytes by synthetic phosphoantigens, zoledronate,

125 During an immune response, CD8+ T lymphocytes can undergo asymmetric division, giving ri

126 hages, and T. cruzi tetramer-specific CD8(+) T lymphocytes capable of producing gamma interferon (IFN

127 ongitudinal analyses of CD3(+), CD4(+) naive T-lymphocyte, CD19(+), and NK-cell numbers from pretrans

128 ther whole blood (WB) or unstimulated CD4(+) T lymphocytes (CD4), and a self-reported asthma control

129 slices and autologous tumor antigen-specific T-lymphocyte clones to provide evidence that CD103 is di

130 neuronal density, perivascular CD3-positive T-lymphocyte clustering, and fibrinogen extravasation we

131 on is accomplishable by recruiting cytotoxic T lymphocytes, concomitant with downregulation of Foxp3(

132 T lymphocytes constitute a major effector cell populatio

133 In this group, CD4+ T-lymphocyte count was low, despite a significantly lowe

134 en-specific cross-presentation and cytotoxic T lymphocyte (CTL) activity.

135 nological synapse formed between a cytotoxic T lymphocyte (CTL) and an infected or transformed target

136 ts an important induction site for cytotoxic T lymphocyte (CTL) immunity to airborne pathogens and in

137 rapamycin treatment did not impair cytotoxic T lymphocyte (CTL) recognition and killing of infected c

138 An effective cytotoxic T lymphocyte (CTL) response against intracellular pathog

139 pecific adaptive immunity, such as cytotoxic T lymphocyte (CTL) response, can result in promising ant

140 Cytotoxic T lymphocyte (CTL)-mediated killing involves the formati

141 ORTANCE In HIV infection, although cytotoxic T lymphocytes (CTL) play a potentially critical role in

142 fficiently cleared by infiltrating cytotoxic T lymphocytes (CTL) without compromising tumor burden.

143 Viral factors (e.g. transmitted cytotoxic T- lymphocyte (CTL) escape mutations) or infant factors

144 for stimulating strong CD8alpha(+) cytotoxic T-lymphocyte (CTL) responses remains lacking.

145 ow that CD8(+) T-cell (also called cytotoxic T lymphocytes, CTL) feedback activates the NLRP3 inflamm

146 itate cytolytic granule release by cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells.

147 erapies are based on the idea that cytotoxic T lymphocytes (CTLs) directly recognize and respond to t

148 CD8(+) cytotoxic T lymphocytes (CTLs) eliminate virally infected cells th

149 boost the anti-tumor responses of cytotoxic T lymphocytes (CTLs) have shown promise; however, clinic

150 l escape of HIV-1 from HIV-1-specific CD8(+) T lymphocytes (CTLs) is a major barrier for effective im

151 l escape of HIV-1 from HIV-1-specific CD8(+) T lymphocytes (CTLs) is a major barrier to effective imm

152 ransfer utilizing tumour-targeting cytotoxic T lymphocytes (CTLs) is one of the most effective immuno

153 Cytotoxic T lymphocytes (CTLs) kill target cells by the regulated

154 Tumor-specific CD8(+) cytotoxic T lymphocytes (CTLs) play a critical role in an anti-tum

155 how cytomegalovirus (CMV)-specific cytotoxic T lymphocytes (CTLs) respond to allogeneic antigen stimu

156 ng clinical-grade BCR-ABL-specific cytotoxic T lymphocytes (CTLs), endowed with antileukemia activity

157 that protects malignant cells from cytotoxic T lymphocytes (CTLs).

158 an be recognized by HIV-1-specific cytotoxic T lymphocytes (CTLs).

159 ciprocal depletion or inactivation of CD4(+) T lymphocytes decreased vessel normalization, indicating

160 us mouse models with vessel normalization or T lymphocyte deficiencies.

161 Combination therapy induced CD8(+) T lymphocyte-dependent primary tumor growth delay and pr

162 -7 expression, while generation of cytotoxic T lymphocytes depends upon T cell receptor-mediated let-

163 istetraprolin-deficient mice after cytotoxic T lymphocyte depletion, but also in WSX-1/tristetraproli

164 ng cells from peripheral blood (particularly T lymphocytes) derived from untreated and 4-6 and 18-26

165 We show that EBV-specific T lymphocytes did not expand properly when stimulated wi

166 uring microbial infection, responding CD8(+) T lymphocytes differentiate into heterogeneous subsets t

167 echanisms by which LFA-1 signaling influence T lymphocyte differentiation into the effector subsets T

168 gammadelta T lymphocytes, dominant T cell subsets in the intestine,

169 the equilibrium of expanding and contracting T lymphocytes during immune response.

170 erations could play a role in sepsis-induced T lymphocyte dysfunction.

171 progression, preferentially localizing near T lymphocytes early in disease and B cells with advanced

172 FATc1 is an important regulator of cytotoxic T lymphocyte effector functions.NFAT nuclear translocati

173 016) showed that forces exerted by cytotoxic T lymphocytes enhance the function of the pore-forming p

174 brain stimulated the proliferation of naive T lymphocytes, enhanced the polarization of T effector c

175 tion by inflammatory cells, particularly Th2 T lymphocytes, eosinophils and basophils into nasal muco

176 Since the 1990s it has been known that B and T lymphocytes exhibit low-level, constitutive signaling

177 e determined the impact of HCA on the CD4(+) T lymphocyte exometabolome and identified potential biom

178 equences of HCA exposure on the fetal CD4(+) T lymphocyte exometabolome.

179 We discovered that: 1) CD4(+) T lymphocytes exposed to HCA exhibit divergent exometabo

180 general unchanged and activated murine B and T lymphocytes express Cyp27b1 Accordingly, elevated spec

181 T lymphocytes express not only cell membrane ORAI calciu

182 ver, plaque-derived beta2GPI-specific CD4(+) T lymphocytes express perforin-mediated and Fas/Fas liga

183 oratory previously showed that NK and CD8(+) T lymphocytes facilitate the pathobiology of septic shoc

184 We reassessed the ability to predict T lymphocyte flow cytometry and complement dependent cyt

185 We cultured naive CD4(+) T lymphocytes from HCA-positive and -negative preterm in

186 T lymphocytes from patients carrying constitutive active

187 After stimulation, T lymphocytes from patients failed to induce glycolysis,

188 y pathway for IL-27 expression and cytotoxic T lymphocyte function mediated by tristetraprolin, contr

189 binding to lymphocytes effectively regulates T lymphocyte function.

190 ate the IFNbeta/CREM/IL-2 axis in regulating T-lymphocyte function during chronic viral infection.

191 However, factors that regulate NK and CD8(+) T lymphocyte functions during sepsis are not well charac

192 sted that in vivo T-cell depletion with anti-T-lymphocyte globulin (ATLG; formerly antithymocyte glob

193 Anti-T-lymphocyte globulin from day -5 to -3 was used for pre

194 munity, including activation of CD8-positive T lymphocytes (GZMA and PRF1) and overexpression of regu

195 marrow (BM)-resident (p190)BCR-ABL-specific T lymphocytes has been correlated with hematologic and c

196 Gut-homing alpha4beta7(high) CD4(+) T lymphocytes have been shown to be preferentially targe

197 In addition to CD4 T lymphocytes, HIV-1 infects tissue macrophages that can

198 ity is not readily detected in resting human T lymphocytes, however upon antigen presentation, telome

199 ls, it appears to operate as an inhibitor of T lymphocyte immune adaptive responses that are not requ

200 CCs to T lymphocytes as a novel approach for T lymphocyte immunomodulation in autoimmune diseases wit

201 single-cell detection of in vitro activated T lymphocytes in flow through an electrical impedance-ba

202 Recent studies suggest a role for T lymphocytes in hypertension.

203 have highlighted the role of differentiated T lymphocytes in psoriasis progression.

204 e encounter of antigen-presenting cells with T lymphocytes in secondary lymphoid organs is essential

205 ) was designed, synthesized, and loaded into T-lymphocytes in order to measure PKB activity in indivi

206 , instead of the more virologically relevant T lymphocytes, in CHO cells; and purifying Env with diff

207 nding patients and longer PFS with increased T-lymphocyte infiltrates, irrespective of PD-1 expressio

208 h disruption of vessel normalization reduced T lymphocyte infiltration as expected, reciprocal deplet

209 with immunostimulatory pathways, especially T lymphocyte infiltration or activity.

210 al vascularization, inhibited trauma-induced T-lymphocyte infiltration (some of which were CD8(+)), a

211 ditis, and MBCD4 signal correlated with CD4+ T-lymphocyte infiltration in the myocardium.

212 junct therapy such as CMV-specific cytotoxic T-lymphocyte infusions.

213 of inflammatory cytokines on NK cell and CD4 T lymphocyte interactions was never investigated.

214 ing the recruitment of CCR9(+)CXCR3(+)CD4(+) T lymphocytes into mouse tumor beds.

215 HF); however, the pathophysiological role of T lymphocytes is unclear.

216 ssion, and glucose entry in septic patients' T lymphocytes, leading to their enhanced proliferation.

217 mmune cells) or specific depletion of CD8(+) T lymphocytes limited osteoblast loss associated with LC

218 cific aortic valve disease (CAVD), activated T lymphocytes localize with osteoclast regions; however,

219 CD8(+) T lymphocytes mediate potent immune responses against tu

220 ernative treatment options for patients with T lymphocyte-mediated diseases.

221 wth of liver metastases, driven by cytotoxic T-lymphocyte-mediated antitumor immunity.

222 s liver carcinogenesis and induces cytotoxic T-lymphocyte-mediated regression of established hepatoce

223 CCR9 expressed on T lymphocytes mediates migration to the small intestine

224 Stiffness modulates T lymphocyte migration and morphological changes induced

225 ntegrin LFA-1 is known to play a key role in T lymphocyte migration, which is necessary to mount a lo

226 PPERS cases demonstrated marked CD3-positive T-lymphocyte, mild B-lymphocyte and moderate macrophage

227 eam signaling cascades, LFA-1 stimulation in T lymphocytes modulates gene-transcription programs, inc

228 terized by unbridled activation of cytotoxic T lymphocytes, natural killer (NK) cells, and macrophage

229 tory cells such as infiltrating macrophages, T lymphocytes, neutrophils, and DCs all contribute to li

230 ssion that is dependent on neither cytotoxic T lymphocytes nor humoral immune response.

231 knockout) leads to a reduction in cytotoxic T lymphocyte numbers.

232 atasi salivary extracts were first tested on T lymphocytes of immune donors.

233 peptides that are recognized by CD4-positive T lymphocytes of Mycobacterium tuberculosis-infected hum

234 e and induce sr39tk expression in platelets, T lymphocytes or cardiomyocytes.

235 Similar to T lymphocytes, PD-1 was upregulated on activated ILCs.

236 L1)-mediated inhibition of activated PD-1(+) T lymphocytes plays a major role in tumor escape from im

237 17 receptor A(-/-) mice were used to examine T-lymphocyte polarization, inflammatory leukocyte recrui

238 latent reservoir for HIV-1 in resting CD4(+) T lymphocytes precludes cure.

239 C3H/HeJ mice were less potent stimulators of T lymphocyte proliferation and TH1/TH17 polarization com

240 less IFN-gamma and TNF-alpha production and T lymphocyte proliferation than in cultures with platele

241 chored, IFN-inducible protein that regulates T lymphocytes proliferation, differentiation, and develo

242 are involved in signaling cascades mediating T-lymphocyte proliferation, differentiation, and migrati

243 and MHC-related molecule-1 (MR1)-restricted T lymphocytes recognize nonpeptidic antigens, such as li

244 evidence that CD103 is directly involved in T-lymphocyte recruitment within epithelial tumor islets

245 B and T lymphocytes residing in the human colonic lamina propr

246 ytes, suggesting a robust adaptive cytotoxic T-lymphocyte response may, in part, confer resilience to

247 tential epitopes that may stimulate a unique T-lymphocyte response to distinguish prior infection wit

248 ctor natural killer (NK) cells and cytotoxic T-lymphocyte responses to leukemia-associated antigens W

249 ivated autoreactive CD8(+) T-cell (cytotoxic T lymphocyte) responses within the islets of patients wi

250 cing approach and analyzed individual CD8(+) T lymphocytes sequentially throughout the course of a vi

251 T-lymphocytes show large changes in ATP demand and nutri

252 Activation of Nfatc1 (-/-) cytotoxic T lymphocytes showed a defective cytoskeleton organizati

253 Patients' T lymphocytes showed increased complement activation cau

254 s, histopathological lesions, and autoimmune T lymphocytes similar to human primary biliary cholangit

255 bind to Tce1 and that this enhancer confers T lymphocyte-specific Gata3 activation in vivo, as targe

256 trated in transgenic mice that Tce1 promoted T lymphocyte-specific transcription of reporter genes th

257 nsfer, to prime the expansion of Ag-specific T lymphocytes, specifically TH17 cells, in vivo.

258 Zebrafish mutant for foxp3a displayed excess T lymphocytes, splenomegaly, and a profound inflammatory

259 atural killer T (iNKT) cells are innate-like T lymphocytes strongly implicated in tumor surveillance.

260 Specifically, neutrophils and CD4(+) T lymphocyte subpopulations were increased, whereas macr

261 Circulating T-lymphocyte subset profiles in conventional HIV- BDD we

262 In parallel, T lymphocyte subsets, as key constituents of the adaptiv

263 No modification of memory T lymphocytes subsets or numbers was observed in the per

264 D8(+), central memory CD4(+), and regulatory T-lymphocyte subsets at enrollment was not associated wi

265 However, the T-lymphocyte subsets involved in the pathophysiology of

266 ntracytoplasmic antigen 1-positive cytotoxic T lymphocytes, suggesting a robust adaptive cytotoxic T-

267 ists, which can activate PI3K selectively in T lymphocytes, synergized with MEK inhibitors in vivo to

268 we applied it to the study of human primary T lymphocytes (T-cells).

269 Among 432 XM with T lymphocytes (T-XM), 407 were analyzed after exclusion

270 Human resting T-lymphocytes, T-lymphoblasts, and the leukemic Jurkat T

271 resenting cells (APC) with sensitized helper T lymphocytes (TC) producing Th2 cytokines may determine

272 The preimmune repertoire consists of mature T lymphocytes that have not yet been stimulated in the p

273 membrane-spanning subunits on the surface of T lymphocytes that initiates cytosolic signaling cascade

274 Circulating T lymphocytes that proliferated and produced tumour necr

275 iant NKT (iNKT) cells are a subpopulation of T lymphocytes that recognize glycolipid antigens in the

276 T reg) cells are a specialized sublineage of T lymphocytes that suppress autoreactive T cells.

277 ed a higher proportion of tumor-infiltrating T lymphocytes (TIL) (n = 24, Mann-Whitney p = 0.047).

278 e molecular correlates of tumor-infiltrating T lymphocytes (TIL) in squamous cell carcinoma (SCC), us

279 eration of both naive and tumor-infiltrating T lymphocytes (TIL).

280 How tumor-infiltrating T lymphocytes (TILs) adapt to the metabolic constrains w

281 en, chronic T cell receptor signaling drives T lymphocytes to a functionally exhausted state.

282 The ability of CD8(+) T lymphocytes to eliminate tumors is limited by their ab

283 onal proliferation of rare, antigen-specific T lymphocytes to form effector cells.

284 D8(+) cytotoxic and CD3(+)CD4(+) helper (Th) T lymphocytes, together with increased Th1, Th2, Th17, a

285 on of IL-12 and increased differentiation of T lymphocytes toward Th1 during infection.

286 nt of the adaptive immune system, using CD4+ T-lymphocyte transcriptomics, would identify gene expres

287 normal VE-cadherin expression and promoting T lymphocyte transmigration.

288 sing a mouse model of AH we assessed whether T lymphocytes undergo activation in the pituitary gland.

289 of naive CD8 T cells into effector cytotoxic T lymphocytes upon antigen stimulation is necessary for

290 T lymphocytes use surface [Formula: see text] T-cell rec

291 roglia and infiltration of CD4(+) and CD8(+) T lymphocytes was observed.

292 hat Ag-specific reactivation of human memory T lymphocytes was prevented.

293 Monocytes and T lymphocytes were stimulated with LPS and PHA, respecti

294 and directly suppress liver cytotoxic CD8(+) T lymphocytes, which prevent emergence of hepatocellular

295 We and others have recently found that T lymphocytes with bound platelets have reduced prolifer

296 peripheral antigen-specific CD8(+) cytotoxic T lymphocytes with immune memory than IFA-emulsifying va

297 a marker, we identified CD4-enriched, mature T lymphocytes with properties of T reg cells.

298 of lysosomes and Pxn at the contact zone of T lymphocytes with rE-cadherin-Fc-coated beads.

299 er a 6-h in vitro activation of naive CD4(+) T lymphocytes with soluble staphylococcal enterotoxin B

300 ltaneous Erk, Jnk and p38 MAPK activation in T lymphocytes within a new immune-inhibitory complex (se