ライフサイエンスコーパス: CD8 T-cell

1 engaging specific subsets of exhausted-like CD8 T cells.

2 infected hepatoma cells against HCV-specific CD8 T cells.

3 the minimal requirement for TCR signaling in CD8 T cells.

4 cell avidity improved antiviral efficacy of CD8 T cells.

5 es and in cross-presenting viral antigens to CD8 T cells.

6 elial cells and neurons and is controlled by CD8 T cells.

7 fector function compared with Cav1 wild-type CD8 T cells.

8 vely expressed on circulating HSV-2-specific CD8 T cells.

9 pressed on human PD1(hi) tumour-infiltrating CD8 T cells.

10 galovirus (CMV), and compared to bulk memory CD8 T cells.

11 riven subset interconversion of human memory CD8 T cells.

12 ed with higher counts of late differentiated CD8+ T cells.

13 tion of PD-L1 by recipient tissues and donor CD8+ T cells.

14 educed naive and effector and central memory CD8+ T cells.

15 In vitro, M2 macrophages inhibit CD4(+) and CD8(+) T cells.

16 tory T cells and greater influx of activated CD8(+) T cells.

17 +), and CCL3(+) polyfunctional, CMV-specific CD8(+) T cells.

18 amma can suppress activation of diabetogenic CD8(+) T cells.

19 in the generation of protective immunity by CD8(+) T cells.

20 necrosis factor-positive CD4(+) T cells and CD8(+) T cells.

21 ATA3, and reduced production of IFN-gamma by CD8(+) T cells.

22 presentation of disease-relevant epitopes to CD8(+) T cells.

23 origin type 1 diabetes-relevant autoreactive CD8(+) T cells.

24 lpha), and interleukin 2 (IL-2) secretion by CD8(+) T cells.

25 , they failed to support activation of naive CD8(+) T cells.

26 creased intracellular Ca(2+) levels in naive CD8(+) T cells.

27 a central regulator of PD-1 transcription in CD8(+) T cells.

28 priming and expansion of cytolytic antiviral CD8(+) T cells.

29 ules to prevent induction of capsid-specific CD8(+) T cells.

30 -9, IL-17, and IL-22 cytokines in CD4(+) and CD8(+) T cells.

31 sition of effector function in ITK-deficient CD8(+) T cells.

32 nti-malarial immunity, mediated primarily by CD8(+) T-cells.

33 % CI = 1.01-2.05; P = .045) and CD38+HLA-DR+ CD8+ T cells (1.40 fold-change in integrated HIV DNA per

34 increased frequency of TRAF1(+) HIV-specific CD8 T cells 10 wk after completion of IL-7 treatment.

35 HIV DNA per 1-unit increase in CD38+HLA-DR+ CD8+ T cells; 95% CI = 1.05-1.86; P = .02).

36 D4(+) T could be inhibited by viral-specific CD8(+) T cells, a result with implications for eliminati

37 Whereas CD8(+) T-cell ablation accelerates hepatocellular carcin

38 In the CT26 model, depletion of CD8(+) T cells abrogated the activity of ADCs when used

39 changes in the Treg population, intratumoral CD8(+) T cells acquired a more functional phenotype char

40 While HCV-specific CD8 T-cell activation with cytolytic and antiviral effec

41 We undertook translatome analysis of CD8 T-cell activation, combining polysome profiling and

42 subsets with biased capacity for CD4(+) and CD8(+) T cell activation are asymmetrically distributed

43 eckpoint molecule that suppresses CD4(+) and CD8(+) T cell activation when expressed on antigen-prese

44 pressing Th1 cell polarization and cytotoxic CD8(+) T cell activation.

45 , and LAG-3 has shown promise for augmenting CD8 T cell activity and boosting pathogen-specific immun

46 ealed that modulating proteasome activity in CD8+ T cells affected cellular metabolism.

47 in more efficient redirection of CD4(+) and CD8(+) T cells against a panel of established blood canc

48 he rapid expansion of adoptively transferred CD8+ T cells against melanoma.

49 n toward a regulatory phenotype and impaired CD8(+) T cell allo-reactive responses, including their a

50 Additionally, both CD8(+) T cells and CD8(+) dendritic cells were identifie

51 f GSK-3alpha/beta reduced PD-1 expression on CD8(+) T cells and limited B16 pulmonary metastasis to t

52 of PD-L1, and contained within their stroma CD8(+) T cells and M1 (antitumor) macrophages.

53 Both antigen-specific CD8(+) T cells and profibrotic cytokines, such as TNFalp

54 circulating and tissue-resident human NK and CD8(+) T cells and promoted the development of tissue-re

55 ction by T1-IFN in human antigen-experienced CD8(+) T cells and provide a mechanism by which the pres

56 imals led to a specific decline in levels of CD8(+) T cells and the rapid reappearance of plasma vira

57 suppression, increases in tumor-infiltrating CD8(+) T cells and tumor cell killing.

58 gulation of CD3, CD8 and CD94, suggests that CD8+ T cells and CD94+ NK cells may play a major role in

59 s were acquired in tumor-infiltrating PD-1hi CD8 T cells, and approaches to reverse these programs im

60 ases in the systemic level of tumor-specific CD8(+) T cells, and an increased ratio of intratumoral C

61 or growth and survival was largely driven by CD8(+) T cells, and immune cell infiltrate in the tumor

62 otoxic infiltrating immune cells, especially CD8(+) T cells, and increased expression of cell prolife

63 onal regulators, some of unknown function in CD8(+) T cells, and that were differentially expressed i

64 he emergence of dysfunctional or 'exhausted' CD8(+) T cells, and the restoration of their functions i

65 interaction of these HRVs with CD4+ T cells, CD8+ T cells, and CD19+ B cells.

66 ure of the interacting receptor expressed by CD8+ T cells, and the tissue environment in which the si

67 While memory CD8(+) T cells are considered a barrier to immunosuppres

68 CD8(+) T cells are important for viral clearance, and al

69 Thus, these results demonstrate that CD8(+) T cells are required for protective immunity agai

70 CD4+ helper T cells and cytotoxic CD8+ T cells are key players for adaptive immune respons

71 ct adhesion and transmigration of CD4(+) and CD8(+) T cells as well as monocytes in an in vitro human

72 ted leukocytes, particularly macrophages and CD8(+) T cells, as well as low expression of genes encod

73 ulfite sequencing of antigen-specific murine CD8 T cells at the effector and exhaustion stages of an

74 including human pan-T cells, CD4(+) T cells, CD8(+) T cells, B cells, and NK cells, with 49 recombina

75 variable E-selectin binding among CD4(+) and CD8(+) T cells but no binding by B cells.

76 reased with the increase of infected time in CD8(+) T cells, but not with that in NK cells, of the pa

77 GRA6Nt is a novel and potent Ag to activate CD8(+) T cells capable of removing T. gondii cysts.

78 From a CD8(+) T cell clone established by stimulation of HLA-A2

79 found that cotransfer of MPO431-439-specific CD8(+) T cell clones exacerbated disease mediated by MPO

80 KK10-stimulated "effective" CD8(+) T-cell clones displayed significantly more rapid

81 mass cytometric cluster analysis of multiple CD8(+) T-cell clones recognizing the identical HLA-B*270

82 responsiveness of effective and ineffective CD8(+) T-cell clones recognizing the identical HLA-B*270

83 Effective and ineffective CD8(+) T-cell clones segregated based on responses to HI

84 e and chemokine secretion than "ineffective" CD8(+) T-cell clones.

85 xpression of CCR10 and CXCR3 by HSV-specific CD8 T cells compared to CD8 T cells specific for control

86 d have low levels of NK cells and CD4(+) and CD8(+) T cells compared to a resistant classical inbred

87 doxorubicin treatment, arguing that cognate CD8(+) T cells contributed to tumor eradication.

88 Low numbers of CD62L-expressing CD4(+) and CD8(+) T cells correlated with higher Sokal score, incre

89 um IgE levels were inversely correlated with CD8 T-cell counts and positively correlated with eosinop

90 ood, Rh-alpha4beta7 increased the CD4(+) and CD8(+) T cell counts, but not B cell counts, and prefere

91 NK/CD8+ T-cell cytotoxicity could play a role in determinin

92 cularly those related to natural killer (NK)/CD8+ T-cell cytotoxicity, separated the 2 groups.

93 gous C51 or CT26 colorectal tumor cells in a CD8(+) T-cell-dependent process.

94 rily to tumor cells, and produces widespread CD8(+) T-cell-dependent tumor cell killing in primary tu

95 t the outcome of PD-L1-mediated signaling in CD8+ T cells depends on the presence or absence of CD4+

96 However, CD8(+) T cell-depleted mice displayed no protection agai

97 CD8(+) T cell depletion in the effector phase of disease

98 vivo after ex vivo PI3K-delta inhibition in CD8(+) T cells destined for adoptive transfer, enhancing

99 se ten-eleven translocation (TET)2 regulates CD8(+) T cell differentiation.

100 Thus, memory CD8 T cells display a preprogrammed chromatin accessibil

101 "pre-memory" cells resulting from the first CD8+ T cell division in vivo exhibited low and high rate

102 in rare cases spontaneously, most antiviral CD8 T cells do not enter B-cell follicles, and those tha

103 trate increased CD30 expression on activated CD8(+) T cells during aGVHD.

104 acologic reduction of proteasome activity in CD8+ T cells early during differentiation resulted in ac

105 Due to their unique combination of CD4 and CD8 T cell effector functions, these CD4(-) CD8alphaalph

106 , we report that maintenance of human memory CD8 T cell effector potential during in vitro and in viv

107 y or STAT5 inhibitor Pimozide led to reverse CD8+ T cell-enhanced BECs proliferation.

108 t diagnosis or at recurrence associated with CD8(+) T cell enrichment.

109 al immunity by regulating natural killer and CD8(+) T cells, epigenetic downregulation of HLA-E by hi

110 c WNT pathway activation was associated with CD8(+) T cell exclusion and VCAN accumulation.

111 This reversal of CD8(+) T-cell exhaustion was dependent on both agonistic

112 Numbers of AH1-specific CD8(+) T cells exhibiting cytotoxic capacity were increa

113 HVEM-deficient CD8 T cells expanded normally but were skewed away from

114 ssion were functional in driving Ag-specific CD8(+) T cell expansion in vitro but that this process w

115 simian immunodeficiency virus (SIV)-specific CD8 T cells express CXCR5 (C-X-C chemokine receptor type

116 The mean percentage of HIV-1 Gag-specific CD8+ T cells expressing interferon gamma increased from

117 loss promotes early acquisition of a memory CD8(+) T cell fate in a cell-intrinsic manner without di

118 can influence the specification of distinct CD8(+) T cell fates, but the observation of equivalent e

119 nes in total splenocytes and in both CD4 and CD8 T cells following immunization with LdCen(-/-) Upon

120 tion site for the recall expansion of memory CD8(+) T cells following influenza virus infection or va

121 of age and sex on gene expression, including CD8(+) T cells for age and CD4(+) T cells and monocytes

122 uto de Pesquisas de Cananeia [p = 0.03]) and CD8(+) T-cell frequency (p = 0.04) correlate with T4 to

123 We report here that CD8(+) T-cell frequency and functional orientation withi

124 ter ex vivo antiviral inhibitory activity of CD8(+) T cells from elite controllers than from HIV-1 pr

125 n as UL47, is a tegument antigen targeted by CD8(+) T cells from HSV-seropositive individuals.

126 CD8(+) T cells from infected mice were polyfunctional an

127 il and lower levels of IL-21R, compared with CD8(+) T cells from normal donors.

128 arker CD57 was significantly up-regulated in CD8(+) T cells from patients with hepatitis delta.

129 he adaptor protein 14-3-3z in the cytosol of CD8(+) T cells from patients with SSc reduces T-bet tran

130 Indeed, SIV-specific, Mamu-E-restricted CD8(+) T cells from RM recognized antigenic peptides pre

131 ion marker expression, restored HIV-specific CD8 T cell function, and led to decreased viral replicat

132 hat downregulate PD-1 expression can enhance CD8(+) T-cell function in cancer therapy to a similar de

133 hat downregulate PD-1 expression can enhance CD8(+) T-cell function in cancer therapy to a similar de

134 r (TCR) clonotypes in differential antiviral CD8(+) T-cell function, we performed detailed functional

135 stimulation in vitro, CXCR5+ but not CXCR5- CD8 T cells generated both CXCR5+ as well as CXCR5- cell

136 CD4 T cells occurred, and peripheral CD4 and CD8 T cells had reduced chemoattractant responses.

137 antibodies (NAbs), their induction of robust CD8 T cells has largely been unreported, even though evi

138 We show that Cav1-knockout CD8 T cells have a reduction in membrane cholesterol and

139 effects of hepatitis C virus (HCV)-specific CD8 T cells have been shown in an HCV replicon system bu

140 IL-13-producing CD8(+) T cells have been implicated in the pathogenesis

141 We found that NKT cells, but not CD4 or CD8 T cells, have dramatically high ROS in the spleen an

142 Virus-specific CD8 T cells home to the site of recurrent infection and

143 CTLA-4 mAb altered MP Treg and MP CD4(+) and CD8(+) T cell homeostasis in a manner similar to that ob

144 plays a fundamental role in the induction of CD8(+) T cell immunity during viral, intracellular bacte

145 that it facilitates the emergence of potent CD8(+) T-cell immunity able to durably suppress virus re

146 CD8(+) T cell immunosurveillance is based on recognizing

147 rovides a proof of principle that suboptimal CD8 T cell in old organisms can be optimized by manipula

148 3 and CCR10, are upregulated on HSV-specific CD8 T cells in blood.

149 n restore TRAF1 expression in virus-specific CD8 T cells in mice, rendering them sensitive to anti-4-

150 3, PD-1, and Tim-3 on virus-specific CD4 and CD8 T cells in relation to their functional T cell profi

151 dent cross-presentation of renal antigens to CD8 T cells in the draining lymph node.

152 eased number and activation state of CD4 and CD8 T cells in the liver and spleen.

153 s the crucial role of effective HIV-specific CD8(+) T cells in controlling HIV-1 replication.

154 increased antiviral capacity of HIV-specific CD8(+) T cells in elite controllers to inhibit HIV infec

155 Subtypes of CD8(+) T cells in insulitic lesions in biopsy specimens

156 Bolstering the apparent feeble numbers of CD8(+) T cells in TG remains a challenge for immunothera

157 opy which demonstrated relative abundance of CD8(+) T cells in the nasopharyngeal mucosa in associati

158 o report a previously unappreciated role for CD8(+) T-cells in mediating rVSV-EBOV protection.

159 nd breast milk cells (BMCs) is increased for CD8+ T cells in both sample sources when compared with C

160 High number of IFNgamma(+) CD8- T cells in the airways was associated with early vi

161 ate the role of TILs, particularly cytotoxic CD8+ T cells, in the prediction of outcomes in patients

162 RNA levels of numerous genes in Nfatc1 (-/-) CD8(+) T cells, including Tbx21, Gzmb and genes encoding

163 d activity of H1N1- and H3N2-specific memory CD8(+) T cells, including tissue-resident cells, compare

164 The frequency of CD39(high)CD8(+) T cells increased with tumor growth but was absen

165 portions of activated cytotoxic NK cells and CD8+ T cells increased significantly during MGN1703 dosi

166 at PPARgamma(High)/RXRalpha(S427F/Y) impairs CD8(+) T-cell infiltration and confers partial resistanc

167 enformin and anti PD-1 cooperatively induces CD8(+) T-cell infiltration and decreases levels of prote

168 ecreased erythema and induration, CD4(+) and CD8(+) T-cell infiltration, and attenuated global gene a

169 n BECs was highly correlated to the level of CD8+ T cell infiltration and the expression of CCL5.

170 The differentiation of naive CD8 T cells into effector cytotoxic T lymphocytes upon a

171 hepatocytes, active migration of Ag-specific CD8(+) T cells into the liver was not observed during th

172 for the importance of HSV-2 antigen-specific CD8 T cells is mounting in animal models and in translat

173 tent antiviral capacity of some HIV-specific CD8(+) T cells is a consequence of factors in addition t

174 dependent on TGF-beta, whereas inhibition of CD8(+) T cells is dependent on TGF-beta and PD-L1.

175 aive wild type and tristetraprolin-deficient CD8(+) T-cells is comparable.

176 Moreover, CD8(+) T cells isolated from lymphoma patients express h

177 of T-bet, GATA-3, and regulatory factors in CD8(+) T cells isolated from the blood and lesional skin

178 s-double-positive, severely exhausted PD-1(+)CD8(+) T cells, leading to reduced tumour burden and imp

179 e we describe a subset of tumor-infiltrating CD8(+) T cells marked by high expression of the immunosu

180 expression and were negative for regulatory CD8(+) T cell markers.

181 in some patients with advanced AIDS, in whom CD8+ T cells may also be depleted.

182 CD8+ T cells may further contribute to trabecular bone l

183 CD8(+) T cells mediate antigen-specific immune responses

184 ity complex (MHC) class I proteins initiates CD8(+) T cell-mediated immunity against pathogens and ca

185 Central to CD8(+) T cell-mediated immunity is the recognition of pe

186 xt of infection influences the generation of CD8(+) T-cell-mediated immune responses.

187 MPECs and development of protective mucosal CD8 T cell memory.

188 actantDeltadriven vectorial migration, while CD8 T cell migration across LEC was not.

189 integrin outside-in signaling that promotes CD8(+) T-cell migratory behavior and effector functions.

190 We hypothesized that CD8(+) T cells modulate calcification in CAVD.

191 Moreover, we identified a pathogenic CD8(+) T cell MPO epitope (MPO431-439) and found that co

192 den, improved lung compliance, and increased CD8(+) T cell numbers in the airways.

193 However, the influence of the recruited CD8+ T cells on BECs under a low androgen level is still

194 eric antigen receptors to genetically modify CD8(+) T cells or bulk T cells for treatment.

195 with ANCA-associated vasculitis suggest that CD8(+) T cells participate in disease, but there is no e

196 Treg and PD-1(+)CD4(+)/CD8(+) T cells persisted in pre-MMR CML patients on TKI.

197 nal state and highlight the heterogeneity of CD8(+) T-cell phenotypes present in chronically inflamed

198 of trigeminal ganglia (TG), and TG-resident CD8(+) T cells play a critical role in preventing its re

199 that an intracellular pool of LFA-1 in naive CD8(+) T cells plays a key role in T cell activation and

200 pletion studies demonstrate that DENV-immune CD8(+) T cells predominantly mediate cross-protective re

201 Indeed, absence of CD8(+) T cells prevented recovery from MRV infection and

202 expression on hematopoietic cells and fewer CD8(+) T cells prior to infection.

203 or viral peptide-exposed eosinophils induced CD8(+) T cell proliferation, activation, and effector fu

204 s providing sufficient help to allow optimal CD8 T cell proliferative responses to exosomal protein.

205 Collectively, these results demonstrate that CD8(+) T cells protect against ZIKV infection.

206 We also detected CD8(+) T cell reactivity against predicted neoepitopes a

207 cid substitutions that result in escape from CD8(+) T cell recognition were not observed, premature s

208 ockdown of TMEM20 in miR-150-deficient naive CD8(+) T cells reduced intracellular Ca(2+) levels.

209 Adoptive transfer of ZIKV-immune CD8(+) T cells reduced viral burdens, whereas their depl

210 uced, long-term expansion of effector memory CD8 T cells, regardless of epitope avidity.

211 numbers of double-positive thymocytes, CD4(+)CD8(-) T cells, regulatory T cells, CD4(+) T cell marker

212 These memory CD8 T cells remain poised to rapidly elaborate effector

213 Analysis of the circulating TCRBV19 CD8 T cell repertoire showed that a majority of NDN-enco

214 Thus, CXCR5+ CD8 T cells represent a unique subset of antiviral CD8 T

215 Brain-infiltrating CD8(+) T cells represent an activated subset of those fo

216 s), conventional CD4(+)Foxp3(-) T cells, and CD8(+) T cells represent heterogeneous populations compo

217 Although effector CD8(+) T cells require <24 h to find, locate, and kill i

218 CD8(+) T cells require sustained Ca(2+) signaling for in

219 unodominance hierarchy, and epitope-specific CD8(+) T cell requirements for costimulation, all of whi

220 with the kinetics of viremia resolution, the CD8 T-cell response was of surprisingly high magnitude a

221 ression had either a delayed or absent PD-1+ CD8 T-cell response, whereas 80% of patients with clinic

222 ccination induced a protective VACV-specific CD8(+) T cell response and protected against a lethal VA

223 el to elucidate the kinetics of the effector CD8(+) T cell response in the liver following Plasmodium

224 The magnitude of the K(d)M282-90 CD8(+) T cell response in TLR agonist-treated neonates c

225 We evaluated the CD8(+) T cell response in ZIKV-infected LysMCre(+)IFNAR(

226 tion with cytomegalovirus (CMV) can elicit a CD8(+) T cell response restricted by the human MHC-Ib mo

227 in CD11c(+) cells, we observed a decrease in CD8(+) T cell response to the L. monocytogenes vaccine.

228 ation dramatically decreased the size of the CD8(+) T cell response to two immunodominant epitopes.

229 apply it to investigate heterogeneity in the CD8+ T cell response in humans and mice, and show that i

230 cells during vaccination impaired protective CD8 T cell responses and ablated sterile protection.

231 e protective vaccine elicited unconventional CD8 T cell responses that were entirely restricted by MH

232 DCs are no longer able to stimulate adequate CD8 T cells responses.

233 While effective CD8 T-cell responses can control viral replication in co

234 tients with clinical benefit exhibited PD-1+ CD8 T-cell responses within 4 wk of treatment initiation

235 Vaccination induced strong mE6 and mE7 CD8(+) T cell responses in all mice, although they were

236 of IL-27 and IL-37 in regulating CD4(+) and CD8(+) T cell responses in S. stercoralis infection.

237 vaccines that induce strong peptide-specific CD8(+) T cell responses in vivo by incorporating an NKT

238 ation ex vivo and defective cross-priming of CD8(+) T cell responses in vivo.

239 ovide a mouse model for evaluating anti-ZIKV CD8(+) T cell responses of human relevance.

240 ur results show that type I IFN can suppress CD8(+) T cell responses to cross-presented Ag by depleti

241 -presentation in DCs is required to initiate CD8(+) T cell responses to dead cells and to induce effe

242 l receptor (TCR) locus that was required for CD8(+) T cell responses to the Plasmodium berghei GAP504

243 HPV-16-specific CD8(+) T cell responses were significantly induced and n

244 hanced and similar HIV-1-specific CD4(+) and CD8(+) T cell responses, similar levels of binding IgG a

245 ls and activate them to prime tumor-specific CD8(+) T cell responses.

246 CD8(+) T-cell responses against the AAV capsid protein c

247 ing that residual Tregs were able to control CD8(+) T-cell responses against the tumor.

248 ymphocyte source and suppressed diabetogenic CD8(+) T-cell responses both directly and through an int

249 8alpha and MyD88 (CD8alpha:MyD88) to enhance CD8(+) T-cell responses to weakly immunogenic and poorly

250 nsistent increase in HDV-specific CD4(+) and CD8(+) T-cell responses was evident when the third signa

251 us neutralizing antibody (nAb) responses and CD8(+) T-cell responses were not significantly enhanced

252 virus both induced and maintained antitumor CD8(+) T-cell responses within directly treated tumors a

253 cally associated with effective Gag-specific CD8(+) T-cell responses.

254 Sequence analysis of T-cell receptors of CD8(+) T cells revealed the presence of H-2L(d)/AH1-spec

255 XCR3 by HSV-specific CD8 T cells compared to CD8 T cells specific for control viruses, Epstein-Barr v

256 upling TRAPeS with transcriptome analysis of CD8+ T cells specific for a single epitope from Yellow F

257 CD8(+) T cell specificity depends on the recognition of

258 Multiple memory CD8(+) T-cell subsets with distinct functional and homin

259 onstituted by adoptive transfer with CD4+ or CD8+ T-cells subsets were reconstituted in T-cell recept

260 ets in tumor-infiltrating, miR-155-deficient CD8(+) T cells, suggesting that miR-155 and ICB regulate

261 Vaccine-induced polyfunctional CD4(+) and CD8(+) T cells targeted 58 (60%) and 15 (16%) of the 97

262 However, a subset of effector CD8(+) T cells (Tc17) produce IL-17 and fail to express

263 (PD-1) and its ligands hamper tumor-specific CD8(+) T cell (TCD8) responses, and PD-1-based "checkpoi

264 factors and steps controlling postinfection CD8(+) T cell terminal effector versus memory differenti

265 Memory CD8 T cells that circulate in the blood and are present

266 cells represent a unique subset of antiviral CD8 T cells that expand in LNs during chronic SIV infect

267 he generation of long-lived antigen-specific CD8(+) T cells that accumulate in mucosal tissues, inclu

268 r inflammation of the skin recruits effector CD8(+) T cells that enter the epidermis and form populat

269 eous B16 melanomas generates tumor-specific, CD8(+) T cells that express PD-1 and suppress tumor grow

270 CD8(+) T cells that express retinoic acid-related orphan

271 E3 ubiquitin ligase Grail is upregulated in CD8(+) T cells that have infiltrated into transplanted l

272 This effect is essential for priming of CD8(+) T cells that mediate systemic tumour rejection (a

273 ted by CD4(+) T cells (P < 0.001 compared to CD8(+) T cells) that coexpressed interleukin-2 (IL-2) (6

274 Among CD4+ and CD8+ T cells, the expression of memory, activation, and

275 mice treated with Cbx3/HP1gamma-insufficient CD8(+) T cells, there is an increase of CD8(+) effector

276 DC subset both expands Tregs and suppresses CD8 T cells to establish an immunosuppressive microenvir

277 ells, and an increased ratio of intratumoral CD8(+) T cells to CD4(+) Tregs.

278 ated CTLs directly activated bystander naive CD8(+) T cells to produce interferon-gamma (IFNgamma) an

279 ted with, an increased recruitment of memory CD8(+)T cells to the liver and exacerbated pro-inflammat

280 al Tregs and M2-like macrophages and reduces CD8+ T cells to promote lung tumor growth.

281 With gliomas, the recruitment of CD8+ T cells to the tumor is impaired, in part preventin

282 These early changes in HCV-specific CD8(+) T cell transcription preceded the overt establish

283 -precursor effector subset of virus-specific CD8 T cells transferred into antigen-free mice revealed

284 CD4(+) and CD8(+) T cells, Tregs, and dendritic cells (DCs) are hig

285 Furthermore, haploidentical donor memory CD8 T cells undergoing in vivo proliferation in lymphode

286 ne production, and the antitumor activity of CD8(+) T cells upon antigenic stimulation.

287 we found that CXCR6 and CCR10 expression by CD8(+) T cells was required for the optimal formation of

288 liferative ability of tumor antigen-specific CD8+ T cells was assessed in the presence of PI3K-alpha,

289 onexhausted TILs and in acutely restimulated CD8(+) T cells, we define a pattern of chromatin accessi

290 y effects of CD200R signaling on transferred CD8(+) T cells, we engineered CD200R immunomodulatory fu

291 tand the mechanisms of memory maintenance in CD8(+) T cells, we performed genome-wide analysis of DNA

292 vitro T cell culture system, MART1-specific CD8 T cells were expanded from healthy donors using arti

293 ntly decreased in the DSS patients, and skin CD8(+) T cells were activated, but there was no accumula

294 breast cancer and melanoma patients, CD39(+)CD8(+) T cells were present within tumors and invaded or

295 Tregs: CD4(+)CD25(-)Fopx3(+)) and CD4(+) and CD8(+) T cells were significantly decreased and increase

296 PD-1 identifies "exhausted" CD8 T cells with impaired HIV-specific effector function

297 lone established by stimulation of HLA-A2(+) CD8(+) T cells with synthetic peptide encompassing the H

298 three lymphocyte cell types (B, CD4+ T, and CD8+ T cells) with high sensitivity and specificity.

299 ntation of Ags and priming the pool of naive CD8(+) T cells within the liver microenvironment.

300 that human LC activation of antigen-specific CD8 T cells would be differentially regulated by epiderm