ライフサイエンスコーパス: T-lymphocyte

1 a direct effect of IL-6 but not IL-1beta on T lymphocytes.

2 of 1095 protein groups from ~130 sorted B or T lymphocytes.

3 mbined immunodeficiency, with no recovery of T lymphocytes.

4 iron homeostasis and lysosomal biogenesis in T lymphocytes.

5 similar levels of B, natural killer, and CD4 T lymphocytes.

6 16L1 T300A phenotypes in dendritic cells and T lymphocytes.

7 eta-cells in a process mediated primarily by T lymphocytes.

8 nt with their cognate receptors on cytotoxic T lymphocytes.

9 luate a subset of the TCRalpha repertoire in T lymphocytes.

10 s, CD30 is expressed on some activated B and T lymphocytes.

11 g of protease-activated receptor 1 (PAR1) on T lymphocytes.

12 40-CD40L interactions between DC1 and CD4(+) T lymphocytes.

13 permits delivery of mRNA into primary human T lymphocytes.

14 ndent transfer of HIV-1 to activated primary T lymphocytes.

15 nted on the cell surface form the targets of T lymphocytes.

16 observed during activation of isolated CD4+ T lymphocytes.

17 and p38 mitogen-activated protein kinase in T lymphocytes.

18 means to redirect the natural properties of T lymphocytes.

19 for activation and persistence of cytotoxic T lymphocytes.

20 ors while promoting the development of B and T lymphocytes.

21 e achieved 8.2 % gene recombination in mouse T lymphocytes.

22 sed activation of antigen-specific cytotoxic T lymphocytes.

23 nd T cell receptor genes in developing B and T lymphocytes.

24 umour-infiltrating natural-killer and CD8(+) T lymphocytes.

25 curtails chemotherapy-induced DNA damage in T-lymphocytes.

26 in the lungs and multifunctional peripheral T-lymphocytes.

27 clear factor of activated T-cells (NF-AT) in T-lymphocytes.

28 eath receptor 1 (PD-1) expressing memory CD4 T lymphocytes (31.7% vs 24.7%, P = .01), and higher plas

29 However, in the case of CD8+ T lymphocytes, a population of unconventional CD44+CD122

30 ) measured at the single-cell level in B and T lymphocytes across patients diagnosed with four major

31 sociated invariant T (MAIT) cells are innate T lymphocytes activated by bacteria that produce vitamin

32 the only antigen-specific interaction during T lymphocyte activation.

33 Infiltration of T lymphocytes, activation of microglia, and their interp

34 ARBs alleviate immunosuppression and improve T lymphocyte activity, enabling dramatically improved re

35 blasts (CAFs) can either suppress or support T lymphocyte activity, suggesting that CAFs may be repro

36 in the test group showed an increase of CD4+ T lymphocytes and a decrease of viral load.

37 ns convey autocrine costimulatory signals to T lymphocytes and can be detected in lymph nodes isolate

38 +) T lymphocytes but fewer numbers of CD4(+) T lymphocytes and CD20(+) B lymphocytes.

39 , intratumoral S100 dendritic cells, and CD8 T lymphocytes and CD57 natural killer cells in the ALNs(

40 ctor molecules expressed by CD8(+) cytotoxic T lymphocytes and function to destroy allogeneic transpl

41 s had significantly increased percentages of T lymphocytes and higher levels of a wide array of infla

42 ned the potential route of EHV1 infection of T lymphocytes and how EHV1 misuses T lymphocytes as a ve

43 en shown to lead to dysfunctional regulatory T lymphocytes and increased proinflammatory macrophages

44 hils in the early fracture hematoma, whereas T lymphocytes and markers for cartilage-to-bone transiti

45 e immune system and is secreted by cytotoxic T lymphocytes and natural killer cells to help eliminate

46 data revealed that NPM-ALK-transformed CD4+ T lymphocytes and primary NPM-ALK+ ALCL biopsies share s

47 Close proximity between cytotoxic T lymphocytes and tumour cells is required for effective

48 HIV-1 primarily infects T lymphocytes and uses these motile cells as migratory v

49 sed flow cytometry to determine the absolute T-lymphocyte and B-lymphocyte counts and the phenotypes

50 Measuring the intraepithelial CD3(+) T-lymphocyte and lamina propria CD138(+) plasma cell den

51 phenotyping showed decreases in naive CD4(+) T-lymphocyte and T helper 17 (Th17) cell percentages, in

52 Active T-lymphocytes and decreased macrophages were present at

53 cal and immune cell kinetics (CD4(+), CD8(+) T-lymphocytes and NK cells in spleen and PBMCs), and apo

54 indicated that CD20(+) B lymphocytes, CD8(+) T lymphocytes, and CD11c(+) cells are susceptible to IAV

55 Monocytes/macrophages, CD4(+) T lymphocytes, and CD20(+) B lymphocytes were increased

56 ntibodies, peripheral blood antigen-specific T lymphocytes, and gene expression in nasal scrapings.

57 ogenic bacteria, remained nonimmunogenic for T lymphocytes, and increased bioavailability in tear flu

58 nvariant T (MAIT), and Vdelta2(+) gammadelta T lymphocytes, and of Mycobacterium-non reactive classic

59 evaluated in activated and quiescent primary T lymphocytes, and the results demonstrated increased in

60 mic stromal cell types, the first developing T lymphocytes, and their possible pre-thymic precursors

61 cell death 1 ligand 1 (PD-L1) and cytotoxic T lymphocyte antigen 4 (CTLA-4) immune checkpoints led t

62 Despite administration of cytotoxic T lymphocyte antigen 4 (CTLA-4) immunoglobulin (Ig), Qa-

63 inhibitors (ICIs), including anti-cytotoxic T lymphocyte antigen 4 (CTLA-4), anti-programmed cell de

64 orts have focused in particular on cytotoxic T lymphocyte antigen 4 (CTLA4) and PD1, both of which ar

65 BACKGROUNDCytotoxic T lymphocyte antigen 4 (CTLA4) is essential for immune h

66 targeting the checkpoint molecules cytotoxic T lymphocyte antigen 4 (CTLA4), programmed cell death 1

67 ve costimulatory molecules such as cytotoxic T lymphocyte antigen-4 (CTLA-4) and programmed cell deat

68 Moreover, upon engaging cytotoxic T lymphocyte antigen-4 (CTLA4), CD80-expressing tSCs dir

69 nfiltrating T lymphocytes, such as cytotoxic T-lymphocyte antigen 4 (CTLA-4) molecules are one of the

70 age-specific effects of CTLA4-Ig (cytotoxic T-lymphocyte antigen 4-Ig), a fusion protein blocking co

71 rammed death receptor-1 (PD-1) and cytotoxic T-lymphocyte antigen-4 (CTLA-4), respectively, on tumor-

72 Anti-cytotoxic T-lymphocyte antigen-4 therapy was associated with incre

73 nts, 17 received therapy targeting cytotoxic T-lymphocyte antigen-4, and 85 received monotherapy targ

74 TIPE-deficient T lymphocytes are completely pilot-less: they are unable

75 controlled effector function of alloreactive T lymphocytes are main drivers of transplant dysfunction

76 nic cell death (ICD) and tumour-infiltrating T lymphocytes are severely weakened by elevated reactive

77 inc supplementation enhances activation when T lymphocytes are stimulated using anti-CD3/anti-CD28 Ab

78 erapy that revives tumour-reactive cytotoxic T lymphocytes, are effective in some patients(1,2), but

79 ection of T lymphocytes and how EHV1 misuses T lymphocytes as a vehicle to reach the endothelium of t

80 +)/TIM-3(+), and CD8(+)/CEACAM-1(+)/TIM-3(+) T lymphocytes as well as CEACAM-1 mean fluorescence inte

81 ot limit infiltration of [Formula: see text] T lymphocytes, as we did not observe significant correla

82 We found de novo expression of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) on CML-LSCs b

83 uction of the checkpoint molecules cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and programme

84 rammed death ligand 1 (PD-L1), and cytotoxic T lymphocyte-associated protein 4 (CTLA-4) for cancer im

85 ed cell death protein 1 (PD-1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4), which limit

86 ed death ligand 1 (PD-1:PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4):B7-1 are amon

87 kpoint inhibitors (ICIs) targeting cytotoxic T lymphocyte-associated protein-4 (CTLA-4) and programme

88 checkpoint inhibitor antibodies to cytotoxic T-lymphocyte-associated antigen 4 (a-CTLA-4) and program

89 e regulators of T-cell activation, cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and programme

90 tolerance was dependent on CTLA-4 (cytotoxic T-lymphocyte-associated antigen-4) signaling.

91 he biophysical interaction between cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and CD80.

92 Blocking antibodies against cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programme

93 ng the immune checkpoint receptors cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programme

94 oxp3 coordinated the regulation of cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) expression le

95 1) and its ligand PD-L1 as well as cytotoxic T-lymphocyte-associated protein 4 (CTLA4) have shown imp

96 nd 2 received a combination of anticytotoxic T-lymphocyte-associated protein 4 and anti-PD-1 antibodi

97 with a panel of CD45, CD28, CTLA4 (cytotoxic T-lymphocyte-associated protein 4), tumor necrosis facto

98 lpha and GSK3beta compared with normal B and T lymphocytes at the messenger RNA and protein levels.

99 ico follow-up suggests a potential effect on T-lymphocytes at HLA-B(*)55:01.

100 CTL-associated protein 4 (CTLA-4), or B and T lymphocyte attenuator (BTLA).

101 of micro entities like healthy human cells (T-lymphocytes, B- lymphocytes, Monocytes, Leukocytes ery

102 erential escape could aid rational cytotoxic T-lymphocyte-based vaccine immunogen selection for both

103 use line is an ideal tool to study cytotoxic T lymphocyte biology and to optimize personalized immuno

104 r capability of delivering mRNA into primary T lymphocytes both ex vivo and in vivo.

105 ial mucosal monocytes/macrophages and CD8(+) T lymphocytes but fewer numbers of CD4(+) T lymphocytes

106 Type I IFN supports cytotoxic T lymphocytes by stimulating the maturation of dendritic

107 The metabolic shift induced in human CD4(+) T lymphocytes by stimulation is characterized by an upre

108 Chimeric antigen receptor (CAR)-redirected T lymphocytes (CAR T cells) show modest therapeutic effi

109 evels increased IL-2 production by activated T lymphocytes, CD25 expression and pSTAT5 levels were de

110 elate well with the populations of cytotoxic T lymphocytes (CD8(+)) and T helper (CD4(+)) cells detec

111 ery of gamma-ketobenzyl-d4TTPs was proven in T-lymphocyte cell extracts.

112 Systemically injected T-lymphocyte cell line Jurkat delivered ICLs to the BM m

113 mune response was investigated by evaluating T-lymphocyte cellularity, cytokine concentration, and vi

114 ty by an enzyme-triggered mechanism in human T-lymphocyte CEM cell extracts loosing first the AB moie

115 y enzyme-triggered reactions in human CD4(+) T-lymphocyte CEM cell extracts.

116 latter compounds were very stable in CD4(+) T-lymphocyte (CEM cell) extracts, and they were substrat

117 In HIV-positive patients, CD4(+) T lymphocytes comprise a well-defined functional latent

118 CD4(+) T lymphocytes consist of naive, antigen-specific memory,

119 Immune T lymphocytes control the replication of Francisella wit

120 We tested whether T lymphocytes could be rendered sensitive to erythropoie

121 CD4 + T-lymphocyte counts are used to assess CD4 + decline and

122 CD4(+) T-lymphocyte counts were <200 cells per microliter in 0/

123 donors, respectively (P = .019), and CD8(+) T-lymphocyte counts were low in 0/20, 4/20, and 11/20 do

124 in CrAg-negative patients with similar CD4+ T-lymphocyte counts.

125 idance by the flow of primary human effector T lymphocytes crawling on substrates coated with ligands

126 These TMPs inhibit cytotoxic T lymphocyte (CTL) activity both in vitro and in vivo, a

127 at induce establish optimal CD8(+) cytotoxic T lymphocyte (CTL) memory for pathogens like the influen

128 al proliferation or HIV-1-specific cytotoxic T lymphocyte (CTL) pressure shape the provirus landscape

129 remodeling, and suppression of the cytotoxic T lymphocyte (CTL) response.

130 Eliciting highly functional CD8(+) cytotoxic T lymphocyte (CTL) responses against a broad range of ep

131 different MxB sensitivities due to cytotoxic T lymphocyte (CTL) selected differences in Gag sequence

132 dules into complexes that redirect cytotoxic T lymphocyte (CTL) specificity and function in response

133 Cytotoxic T lymphocyte (CTL)-based cancer immunotherapies have sho

134 Vaccines that induce cytotoxic T lymphocyte (CTL)-mediated immune responses constitute

135 CD8(+) cytotoxic T lymphocytes (CTL) and natural killer cells are the mai

136 Although CD8(+) antitumor cytotoxic T lymphocytes (CTL) are the preferred effectors of cance

137 med cell death protein 1 (PD-1) on cytotoxic T lymphocytes (CTL) in colon cancer.

138 We postulate that enhancing cytotoxic T lymphocytes (CTL) targeting conserved envelope (Env) r

139 signature, and the ratio of CD8(+) cytotoxic T lymphocytes (CTL) to CD68(+) macrophages both predict

140 ding of the mechanisms employed by cytotoxic T lymphocytes (CTL) to control tumors will aid in the de

141 sion (RIS), rituximab (from 2000), cytotoxic T-lymphocyte (CTL) therapy (available in 1999-2004 and f

142 sed infiltration and activation of cytotoxic T lymphocytes (CTLs) and CD103+ cross-presenting dendrit

143 tolytic lymphocytes-including CD8+ cytotoxic T lymphocytes (CTLs) and natural killer cells-and regula

144 trophil NETs interfering cytolytic cytotoxic T lymphocytes (CTLs) and NK cell contacts with tumor cel

145 ological synapse formation between cytotoxic T lymphocytes (CTLs) and the target cells they aim to de

146 Cytotoxic T lymphocytes (CTLs) are thought to arrive at target sit

147 in vivo molecular imaging of CD8+ cytotoxic T lymphocytes (CTLs) in response to anti-PD-L1 therapy.

148 Cytotoxic T lymphocytes (CTLs) kill infected and cancerous cells.

149 owever, that DC vaccine priming of cytotoxic T lymphocytes (CTLs) requires the activity of endogenous

150 roteins also occurs from activated cytotoxic T lymphocytes (CTLs) where they have recently been repor

151 Cytotoxic T lymphocytes (CTLs) with strong abilities to suppress H

152 cells to evade killing mediated by cytotoxic T lymphocytes (CTLs), we performed genome-wide CRISPR sc

153 targeting and specific binding to cytotoxic T lymphocytes (CTLs).

154 rimary breast tumors, they exclude cytotoxic T lymphocytes (CTLs).

155 -I) expression to evade killing by cytotoxic T lymphocytes (CTLs).

156 Cytotoxic T-lymphocytes (CTLs) and natural killer cells (NKs) kill

157 Type II IFN (IFN-gamma) is a proinflammatory T lymphocyte cytokine that serves in priming of microgli

158 pressive cells, the improved cytotoxicity of T lymphocytes, decreased inhibitory and increased inflam

159 my is the capacity of the thymus to maintain T lymphocyte development and export independently of bon

160 Naive CD4(+) T lymphocytes differentiate into various Th cell subsets

161 hronic infection with SFV is associated with T lymphocyte differentiation and monocyte activation.

162 peutic applications, were shown to stimulate T lymphocytes directly and at relatively low-exposure do

163 wever, delivering large biologics to primary T lymphocytes directly in vivo is technically challengin

164 Psoriasis is a T lymphocyte-driven systemic inflammatory disease.

165 sfer of donor-derived EBV-specific cytotoxic T-lymphocytes (EBV-CTLs) can eradicate EBV-associated ly

166 ary mechanisms by which LXRalphabeta governs T lymphocyte education and illuminate LXRalphabeta's ind

167 Here we show that activated T lymphocytes efficiently become infected and support vi

168 CEACAM-1), a molecule expressed on activated T lymphocytes, endows TIM-3 with inhibitory function and

169 Both receptors could be expressed in human T lymphocytes; Epo ligation induced STAT5 phosphorylatio

170 The T lymphocyte, especially its capacity for antigen-direct

171 et of genes that are associated with stromal T-lymphocyte exclusion.

172 While both B and T lymphocytes exhibit memory responses, this review disc

173 Albeit T-lymphocytes express all classes of viral proteins earl

174 able tumor mass invasion by cytotoxic CD8(+) T lymphocytes, following the Pt(IV) treatment, indicated

175 ch can activate latent HIV-1 in resting CD4+ T lymphocytes from antiretroviral treated HIV-1 infected

176 Moreover, encephalitogenic T lymphocytes from IFN-alpha-treated mice re-exposed to

177 Moreover, both CD4(+) and CD8(+) T lymphocytes from Mtb infected, metformin treated anima

178 tumoral infiltration of macrophages and CD8+ T lymphocytes, granzyme B production by cytotoxic cells

179 Specific populations of T lymphocytes have emerged as important reparative cells

180 teractions occurring between tumor cells and T lymphocytes; however, recent data highlight a crucial

181 s (GE KER), dendritic cells (DC), and helper T lymphocytes (HTL) exposed to lipopolysaccharide (LPS)

182 In T lymphocytes, hypozincemia promotes thymus atrophy, pol

183 ture that demonstrates how cytokines made by T lymphocytes impact the gastric epithelium, especially

184 nd deep characterization of human gammadelta T lymphocytes in further scRNA-seq studies of complex ti

185 hils and neutrophils only in COPD and CD8(+) T lymphocytes in patients with COPD and nonsmokers.

186 ested by an accelerated decline of the naive T lymphocytes in pDGS as well as a more skewed T-cell re

187 nalysis to quantify TCR-Valpha7.2-expressing T lymphocytes in peripheral blood and developed PROMIDIS

188 ta T cells, accounting for 0.5% to 5% of all T lymphocytes in the peripheral blood and lymphoid tissu

189 tic cells efficiently transferred virions to T lymphocytes in the presence of neutralizing antibodies

190 maturation and the infiltration of cytotoxic T lymphocytes in tumor.

191 tion of typical T(H) 2 cytokines in Asm(-/-) T lymphocytes in vitro.

192 ted liver injury revealed an infiltration of T-lymphocytes in areas of hepatocellular damage.

193 Lymphocyte, especially T lymphocyte, in severe and critical patients showed a d

194 Here, we found that activated CD8(+) T lymphocytes infiltrate the central nervous system (CNS

195 e inflamed subtype (11%) presented a massive T lymphocyte infiltration, an activation of inflammatory

196 e inflamed subtype (11%) presented a massive T-lymphocyte infiltration, an activation of inflammatory

197 derive from pre-existing tumor-infiltrating T lymphocytes; instead, the expanded clones consisted of

198 lecules promote differentiation of naive CD4 T lymphocytes into helper T cells subtypes, including ty

199 Implantation of NPM-ALK-transformed CD4+ T lymphocytes into immunodeficient mice resulted in the

200 inflammatory cells including neutrophils and T lymphocytes into the skin and hyperkeratosis/hyperplas

201 Engineering T lymphocytes is an emerging approach in a variety of bi

202 IL-3, a cytokine secreted by activated T lymphocytes, is known to regulate the proliferation, s

203 s Review focuses on the major populations of T lymphocytes known to mediate tissue repair, their repa

204 Patient T lymphocytes lacked surface expression of IL-2Rbeta and

205 Most T lymphocytes leave the thymus as naive cells with limit

206 tokines release (cytokine storm) and loss of T lymphocytes (leukopenia) characterize the most aggress

207 nventional T cells, a heterogeneous class of T lymphocytes (MAIT, gammadeltaT, and iNKT cells) with p

208 In T lymphocytes, MAL is found at the immunological synapse

209 mphoid organ that plays an essential role in T lymphocyte maturation and selection during development

210 e achieved with immunotherapy that relies on T lymphocyte-mediated recognition of tumor antigens.

211 Immune activated T lymphocytes modulate the activity of key metabolic pat

212 T lymphocyte motility and interaction dynamics with othe

213 ivated and tissue-resident memory (TRM) CD8+ T lymphocytes, myeloid-derived suppressor cells (MDSCs),

214 ntegrin beta7(+) natural gut intraepithelial T lymphocytes (natural IELs)-that is dispersed throughou

215 ompanied by increase in the number of CD8(+) T lymphocytes, NK cells, and CD11b(+) cells in SLR14-tre

216 Latest CD4+ T-lymphocyte number was significantly lower in transplan

217 vitro data, in vivo AQP4 inhibition reduced T lymphocyte numbers in the lymph nodes with simultaneou

218 The reduction in intraepithelial T lymphocytes occurs within 7 wk of high-fat diet admini

219 c protein (MBP)-stimulated CD4(+) and CD8(+) T lymphocytes of 56 MS patients with a diagnosis of eith

220 lphabetaTCR is identified from the cytotoxic T lymphocytes of patients with carbamazepine-SJS/TEN, wi

221 w report that mice deficient in conventional T lymphocytes or recombination-activating gene (Rag) fai

222 ) production (P = 0.0215) but did not affect T lymphocyte (P = 0.0796).

223 368 HIV-negative MSM and 72 HIV-negative MSW T-lymphocyte phenotyping was performed 3 times bienniall

224 Tumor-infiltrating CD8-positive (CD8+) T lymphocytes play a central role in antitumor immune re

225 d innate T (MAIT) cells, are a heterogeneous T lymphocyte population with effector properties preprog

226 lly, we identify subsets of granulocytes and T lymphocytes present in all wounds paving the way for s

227 t wild type thymi maintain their function of T lymphocyte production upon transplantation into recipi

228 or multiple fundamental processes that drive T lymphocyte proliferation and differentiation.

229 which several compounds showed inhibition of T-lymphocyte proliferation at levels equal or superior t

230 yte proliferation (P = .041), and lower CD4+ T lymphocyte proportion (P = .032).

231 Low total helper T lymphocyte proportions and low naive helper T cell pro

232 Reltecimod, a CD 28 T-lymphocyte receptor mimetic, inhibits T-cell stimulati

233 an emphasis on the fundamental importance of T lymphocyte regulation.

234 Absolute numbers of T lymphocytes remained within normal limits throughout t

235 In the thymus, the T lymphocyte repertoire is purged of a substantial porti

236 s critical for central tolerance and diverse T-lymphocyte repertoire development, to provide lifelong

237 The patients' primary B and T lymphocytes responded poorly to STAT3-dependent cytoki

238 been shown to effectively mount a cytotoxic T lymphocyte response through enhanced tumor immunogenic

239 ted a TMP-specific H-2K(b)-restricted CD8(+) T lymphocyte response upon immunotherapy with cyclophosp

240 of subjects developed VSV-specific cytotoxic T-lymphocyte responses and antibodies.

241 ph nodes induce activation of tumor-specific T-lymphocyte responses that can result in cytolytic targ

242 umour immunity and increased infiltration of T lymphocytes, resulting in highly potent antitumour eff

243 e viral outgrowth assays from peripheral CD4 T lymphocytes show no reactivatable virus using a total

244 oantigen and anti-CD3/CD28 stimulated CD4(+) T lymphocytes showed higher expression of a cluster of 5

245 However, they are the most abundant T-lymphocyte subset in some epithelial barriers such as

246 the differentiation and function of several T lymphocyte subsets that provide immunity to infection,

247 reconstituted different quantities of CD4(+) T lymphocyte subsets with preferential expansion of CXCR

248 nt molecules expressed on tumor-infiltrating T lymphocytes, such as cytotoxic T-lymphocyte antigen 4

249 n-classical monocytes, and subsets of NK and T lymphocytes, suggesting extravasation to affected tiss

250 ed for smooth muscle cells, macrophages, and T lymphocytes, suggesting that these cells have multiple

251 CR clonal diversity among tumor-infiltrating T lymphocytes, supporting a local immunomodulatory effec

252 auses breast cancer cells to evade cytotoxic T-lymphocyte surveillance, which leads to tumor growth.

253 een investigated in detail; CD4(+) cytotoxic T lymphocytes (suspected of promoting disease) and a spe

254 act with antigen-presenting cells, cytotoxic T lymphocytes (T cells) establish a highly organized con

255 replication in human macrophages and CD4(+) T lymphocytes (T cells).

256 ed individuals, but whether stem cell memory T lymphocytes (T(SCM)) contribute to such attrition is s

257 Cytotoxic T lymphocytes (T) and natural killer cells are the main

258 asis, and differentiation into CD4(+) helper T lymphocyte (Th)17 cell phenotypes.

259 had a significantly higher percentage of CD8 T lymphocytes than controls (median, 17.6% vs 13.7%; P =

260 mune cells and more immune cells, especially T lymphocytes, than control tissues did.

261 rotein 1 (PD-1) is an inhibitory receptor on T lymphocytes that is critical for modulating adaptive i

262 is a cell surface receptor present on B and T lymphocytes that is universally and strongly expressed

263 In T lymphocytes, the Wiskott-Aldrich Syndrome protein (WAS

264 In contrast to conventional T lymphocytes they recognize lipid antigens.

265 those used to reactivate tumor-infiltrating T lymphocytes (TIL), for example, by cytokines or immune

266 ic epitopes recognized by tumor-infiltrating T lymphocytes (TILs) from eight melanoma patients for al

267 and antitumor activity of tumor-infiltrating T lymphocytes (TILs).

268 tegy to allow transfer of progeny virus from T lymphocytes to adjacent target cells.

269 mpairing cytotoxicity, excess IL-18 acted on T lymphocytes to amplify their inflammatory responses.

270 resistance of hematopoietic progenitors and T lymphocytes to DNA cross-linking agents.

271 hat tumors induce de novo steroidogenesis in T lymphocytes to evade anti-tumor immunity.

272 For CD8 T lymphocytes to mount responses to cancer and virally-i

273 ce have a marked defect in positioning their T lymphocytes to various tissues, both at the steady-sta

274 s as a thermal sensory pathway that promotes T lymphocyte trafficking and enhances immune surveillanc

275 g histone methylation could enhance effector T lymphocyte trafficking and improve therapeutic efficac

276 ndicate that blocking AQP4 reversibly alters T lymphocyte trafficking pattern.

277 ng lipidoids that are particularly potent in T lymphocytes transfection.

278 previously identified as monocytic cells and T lymphocytes, transmit EHV1 to endothelial cells of the

279 Regulatory T lymphocytes (Treg) play an important role in preventin

280 Regulatory T lymphocytes (Tregs) display immuno-suppressive mechani

281 s intervention induces functional regulatory T lymphocytes (Tregs) in mouse lung experimentally infla

282 Regulatory T-lymphocytes (Tregs) are considered key suppressors of

283 educed numbers of F4/80 macrophages, and CD3 T-lymphocytes upon LP treatment.

284 l other NCRs that are expressed on activated T lymphocytes, V-type immunoglobulin domain-containing s

285 The total lymphocyte count, CD4+ and CD8+ T lymphocytes values were lower in the cases than in the

286 Co-localization of B- and T-lymphocytes was observed.

287 Antigen-specific B and T lymphocytes were analyzed in an adoptive transfer airw

288 with aTB, HBHA-specific polycytotoxic CD4(+) T lymphocytes were detected in LTBI subjects and not in

289 ries of TCRVdelta1 and TCRVdelta2 gammadelta T lymphocytes were discovered, unveiling in both subsets

290 ACAM-1 mean fluorescence intensity on CD4(+) T lymphocytes were significantly reduced; 2) apoptotic C

291 (+)/CEACAM-1(+) and CD8(+)/AV(+)/CEACAM-1(+) T lymphocytes were significantly reduced; and 3) Bat3-ex

292 st that L. reuteri secreted factors regulate T-lymphocytes which play an important role in mediating

293 eracted directly with infiltrating cytotoxic T lymphocytes, which led to macrophage depletion.

294 ul generation and characterization of Jurkat T lymphocytes with deletions in CD18, CD11a, and Fas tha

295 which are viable and fertile, have cytotoxic T lymphocytes with endogeneously fluorescent cytotoxic g

296 During contact of infected T lymphocytes with endothelial cells, a late viral prote

297 t in vitro transduction of normal human CD4+ T lymphocytes with NPM-ALK results in their immortalizat

298 The interaction of CD8(+) T lymphocytes with tumor cell spheroids in vitro induced

299 tion protects them from killing by cytotoxic T lymphocytes, yet dampens the antitumor responses.

300 al that sorting the most migratory cytotoxic T lymphocytes yields a pool of cells with enhanced cytot