ライフサイエンスコーパス: T cell

1 activity of chimeric antigen receptor (CAR) T cells.

2 rticular, ET were enriched in polyfunctional T cells.

3 ntigen-presenting cells (aAPCs) and reporter T cells.

4 gen-mediated signals to human Vgamma9Vdelta2 T cells.

5 is in Fcgr2b(+), but not Fcgr2b(-/-), CD8(+) T cells.

6 plication-competent virus cultured from CD4+ T cells.

7 ements drive gene expression in primary CD4+ T cells.

8 ral Ags, and all patients had Spike-specific T cells.

9 cted peptides targeted by circulating CD8(+) T cells.

10 e and impaired recruitment and activation of T cells.

11 plasma cells, and activation of CD4 and CD8 T cells.

12 ed by the constant degranulation of Gal-9(+) T cells.

13 epertoire diversity of virus-specific CD8(+) T cells.

14 atory objectives included tracking of edited T cells.

15 opic cytokine produced predominantly by CD4+ T cells.

16 NOD-PerIg CD8(+) T cells but required CD4(+) T cells.

17 rain has the unique ability to infect mature T cells.

18 tion of CD68/CD206 on MNPs and CD69/CD103 on T cells.

19 ursors of M2 macrophages, DCs and regulatory T cells.

20 f pathogenic IL5(+) IL17A(+) CD4(+) effector T-cells.

21 Nuclear Factor of Activated T cells 5 (NFAT5) is a transcription factor (TF) that me

22 findings define AP-1 as the key link between T cell activation and chromatin remodeling.

23 pinocytosis that increases in magnitude upon T cell activation to support T cell growth even under am

24 a global stabilization of spliced mRNAs upon T cell activation, although the stability of intron-reta

25 I and III responses, early CD4(+) and CD8(+) T cell activation, and counterregulation by the co-recep

26 al and adipose cells and how it promotes CD8 T cell activation, as well as epithelial repair.

27 Noninvasive strategies detecting T-cell activation would allow for early diagnosis and po

28 Loss of Yap in T cells results in enhanced T-cell activation, differentiation, and function, which

29 ance and immunopathology associated with CD8 T cell activity in the CNS.

30 rtance of inappropriate NOTCH1 signalling in T-cell acute lymphoblastic leukaemia (T-ALL), and the in

31 of RSV-F-specific interferon gamma-secreting T-cells after a ChAd155-RSV high dose was 108.3/106 PBMC

32 ld and a conceptually simple model of CD8(+) T cell Ag recognition, in which Ag dose and affinity do

33 All patients had reactive T cells against at least 1 of 12 analyzed viral Ags, and

34 ) APCs are critical for early priming of CD8 T cells against the immunodominant TMEV peptide VP2(121-

35 When a T cell and an antigen-presenting cell form an immunologi

36 ity and antitumoral capacity of NK cells and T cells and downmodulated Treg cell activities.

37 ed an increased PD-1 and PD-L1 expression in T cells and monocytes, respectively, which was linked to

38 ssing and priming for both CD4(+) and CD8(+) T cells and of the direct orchestration of their cross-t

39 Inhibition of NOX4 increased CD8(+) T cells and restored responsiveness to immune therapy, s

40 about the immune functions of unconventional T cells and their role in hypersensitivities.

41 gic T-bet(-)IFN-gamma(-) phenotype in CD8(+) T cells and was equally suppressive compared to PD-1 sig

42 tics comparable to influenza-specific CD8(+) T cells and were detectable in SARS-CoV-2 convalescent i

43 ffinity analyses of cytomegalovirus-specific T cells, and through the generation and in vivo monitori

44 sting and induced SARS-CoV-2-specific CD8(+) T cells, applying peptide-loaded major histocompatibilit

45 In conclusion, orchestrated T cells are able to regulate osteoclasts at the early st

46 mary, the current study suggests that CD4(+) T cells are critical for controlling acute-stage poliomy

47 Although CD4+ T cells are implicated in MS pathogenesis and have been

48 hlight new evidence indicating that neonatal T cells are not inert or less potent versions of adult T

49 cell receptor (TCR)-transgenic T cells (TCR-T cells) are not restricted by cell surface expression o

50 tional IFN-gamma-producing CD107(ab+) CD4(+) T cells associated with protective immunity against ocul

51 n contrast, increased frequency of EM CD8(+) T cells associated with reduced risk of graft failure.

52 IV DNA isolated from peripheral blood CD4(+) T-cells at weeks 16 and 18 after randomisation.

53 ons/glia for the brain data and granulocytes/T cells/B cells/monocytes for the blood data.

54 munotherapy and has general implications for T cell-based immunotherapies.

55 ngs are important for the improvement of CAR-T cell-based immunotherapy for human cancers.

56 f transiently inhibiting LDH during adoptive T cell-based immunotherapy, with an unanticipated cooper

57 n about the thymus and some of its products, T cells bearing alphabeta receptors for antigen.

58 responses through altering LN structures and T cell behaviors.

59 e not inert or less potent versions of adult T cells but instead are a broadly reactive layer of T ce

60 developed in the absence of NOD-PerIg CD8(+) T cells but required CD4(+) T cells.

61 activity is linked to T-bet in Ag-expCD4(+) T cells but that reduction in mTOR activity may not dire

62 th factor-beta receptor 2 (TGFBR2) in CD4(+) T cells, but not CD8(+) T cells, halts cancer progressio

63 s pronounced in perivascular and circulating T cells, but not in perivascular adipose tissue adipocyt

64 Activation of cytotoxic CD8(+) T cells by cross-priming DC contributes to exacerbation

65 e cancer- and virus-induced exhausted CD8(+) T cells, by enhancing the quality and survival of immune

66 Activation of gammadelta T cells can be elicited by butyrophilin and butyrophilin

67 hus, purinergic signaling in differentiating T cells can be targeted to improve vaccine responses, in

68 However, CAR T cells can induce substantial toxic effects, and the ma

69 T cells can sometimes acquire properties of a memory cel

70 Is) after chimeric antigen receptor-modified T-cell (CAR-T-cell) therapy are limited.

71 gamma-delta T cells (CD3(+)TCRgd(+)), CD8(+) T cells (CD3(+)CD8(+)CD161(+)PD1(+)), and memory B cells

72 Subsets of gamma-delta T cells (CD3(+)TCRgd(+)), CD8(+) T cells (CD3(+)CD8(+)CD

73 ed the phenotype characteristics of effector T cells (CD45RA(+), CD45RO-/lo, CD62L(-), CD27lo) with h

74 rly clonal dynamics imprint the hierarchy of T cell clone sizes with implications for pathogen defens

75 nd that the immunodominance of high-affinity T cell clones declined during the chronic infection phas

76 tection of atabecestat metabolite-responsive T-cell clones activated via a pharmacological interactio

77 These data show that HTLV-1-infected T-cell clones carrying key oncogenic driver mutations ca

78 abacavir/abacavir analogue-responsive CD8(+) T-cell clones was measured using IFN-gamma ELIspot.

79 in Tph1 deficient ILC2s including inducible T cell co-stimulator (Icos).

80 with this hypothesis, mice transplanted with T-cells co-expressing NOTCH1 and NRARP develop leukemia

81 Although T cell commitment is accompanied by large scale epigenet

82 comorbidity had larger numbers of activated T cells compared with patients who had fewer risk factor

83 an unexpected heterogeneity within the naive T cell compartment in mice, where loss of VISTA disrupte

84 udies, we find that human blood sLeX(+)CD4(+)T cells comprise a subpopulation expressing high levels

85 ngs demonstrate that STAT1 signaling and CD8 T cells concomitantly act to mitigate MuPyV-encephalopat

86 cific cytokines produced by autoreactive CD4 T cells contribute to the pathogenesis of MS.

87 the possibility that proinflammatory CD151+ T cells could contribute to the premature immunological

88 that persists despite HIV-specific cytotoxic T cell (CTL) responses.

89 rforin contributed to both CD8+ and CD4+ CAR T cell cytotoxicity but was not required for in vitro or

90 generation Chimeric Antigen Receptors (CAR) T cells demonstrating specific cytolytic activity.

91 rate that alphaCD3 alone induced substantial T-cell depletion, impacting both conventional T cells (T

92 CD4+ T cells derived from individuals with latent Mtb infecti

93 role of the different subsets of gammadelta T-cells detected in the skin in steady-state, psoriasis,

94 transfer studies indicate that these memory T cells develop in a cell-intrinsic manner following thy

95 amily kinase Lck plays critical roles during T cell development and activation, as it phosphorylates

96 ions harboring genes with prominent roles in T cell development in both strains.

97 te Notch, a critical regulator of B cell and T cell development.

98 role for LDH in modulating cytokine-mediated T cell differentiation and underscore the therapeutic po

99 s are constitutively unmethylated throughout T cell differentiation, irrespective of their activation

100 d priming in identifying novel regulators of T cell differentiation.

101 This can complement existing T cell-directed immunotherapy, providing a promising app

102 traepithelial CD8(+) T-cell lines, or CD8(+) T cells directly isolated from intestinal biopsies, with

103 r virus (EBV) is associated with a number of T-cell diseases, including some peripheral T-cell lympho

104 The glycopeptide specific CD4(+) T cells display a prominent feature of Th2 and Th17 diff

105 Upon IL-6 treatment, Endo-N and Endo-T cells displayed altered expression of the DNA methyltr

106 c predisposition, epidermal dysfunction, and T-cell driven inflammation.

107 essed on highly functional ganglionic CD8(+) T cells during acute and latent HSV-1 infection.

108 a, we develop a quantitative theory of human T cell dynamics compatible with the statistical laws of

109 cells for metabolic resources often renders T cells dysfunctional.

110 R signal strength is able to regulate CD8(+) T cell effector cytokine R production independent of TCR

111 -presentation, that CD40L-overexpressing CAR T cells elicit an impaired antitumor response in the abs

112 r vaccinia virus (VV) stimulation to measure T cells elicited after childhood smallpox vaccination.

113 Here we show that primary mouse and human T cells engage in macropinocytosis that increases in mag

114 he absence of endogenous PD-L1; (3) PD-L1(+) T cells engaged PD-1(+) macrophages, inducing an alterna

115 Bispecific T cell engagers have demonstrated clinical efficacy; how

116 Conversely, lack of CD137L on T cells enhanced their diabetogenic activity.

117 e reasons, a cataloging and appraisal of the T-cell epitopes targeted in type 1 diabetes was complete

118 T cell exhaustion represents one of the most pervasive s

119 SARS-CoV-2-specific memory CD8(+) T cells exhibited functional characteristics comparable

120 Gal-9(+) T cells exhibited the phenotype characteristics of effec

121 T cell expansion and differentiation are critically depe

122 proach is often limited by the extent of CAR-T cell expansion in vivo.

123 estinal barrier dysfunction could facilitate T cell exposure to commensal/pathogenic microbes.

124 to MCC cells with restored STING, cocultured T cells expressing MCPyV-specific T cell receptors (TCRs

125 gG, IgG3 binding, and neutralizing) and CD4+ T-cell (expressing interferon-gamma, interleukin-2, and

126 ir intact cGAS sensing pathway, human CD4(+) T cells failed to mount a reverse transcriptase (RT) inh

127 g of the Th1/Th2 paradigm ignited the CD4(+) T cell field.

128 B22M2C, a radiolabeled minibody against CD8+ T cells, for targeted imaging of CD8+ T cells in patient

129 ctivity, had significantly higher CD4+CD151+ T-cell frequencies than healthy controls, raising the po

130 T cells from infant mice were predominantly immature, in

131 rectly or indirectly excluding effector CD8+ T cells from the tumor microenvironment.

132 To understand how these compounds alter T cell function, we assessed their therapeutic activity

133 magnitude upon T cell activation to support T cell growth even under amino acid (AA) replete conditi

134 The vaccine-induced T cells had a cytotoxic phenotype and were capable of tr

135 In those whose T cells had the capacity to respond, older patients with

136 2 (TGFBR2) in CD4(+) T cells, but not CD8(+) T cells, halts cancer progression as a result of tissue

137 CAR-T cells have shown encouraging activity against recurren

138 art, on their ability to effectively recruit T cell help after B cell activation.

139 ssue and is related to the B7/CD28 family of T-cell immune checkpoint markers.

140 tages of tumor inception to subvert adaptive T cell immunity.

141 function of FcgammaRIIB in regulating CD8(+) T cell immunity.

142 regnancy is associated with recovery of CD4+ T cell immunity.

143 on in complex biological settings, including T cell immunology.

144 ition to suppressing viremia, bNAbs may have T cell immunomodulatory effects as seen for other forms

145 We were able to detect SARS-CoV-2-specific T cells in 10 of 10 COVID-19 patients with mild symptoms

146 mixed phenotype of apoB-reactive autoimmune T cells in atherosclerosis and suggest an initially prot

147 m patients with MS points to a role for CD8+ T cells in disease pathogenesis.

148 ich are then eradicated by CD19-specific CAR-T cells in immunodeficient and immunocompetent mouse mod

149 ppress the activity of pancreas autoreactive T cells in newly hyperglycemic non-obese diabetic (NOD)

150 t CD8+ T cells, for targeted imaging of CD8+ T cells in patients with cancer.

151 pands the proportion of proliferating CD8(+) T cells in the tumor with enhanced cytolytic potential a

152 We have examined the priming of naive CD4 T cells in vitro at fever temperatures, and we report no

153 )CD8(-)TCRalphabeta(+), double-negative (DN) T cells, in mouse secondary lymphoid organs.

154 eat me" signal for macrophages) and PD-L1 (a T-cell inactivator) on their surface.

155 neages of intestinal antigen-specific CD8(+) T cells, including a Blimp1(hi)Id3(lo) tissue-resident e

156 al cancer-specific neoantigens that activate T-cells indicating that they are cancer vaccine candidat

157 However, whether T cells induced by one viral species cross-react with ot

158 nd neoantigen load) and the degree of CD8(+) T cell infiltration were not associated with clinical re

159 ith lower levels of Th1 cytokines, decreased T cell infiltration, increased B cell numbers, and decre

160 dothelial ICAM-1 and VCAM-1 was confirmed by T-cell interaction with EECM-BMEC-like cells.

161 ctional consequence of LEC priming of CD8(+) T cells is unknown.

162 PD-L1 pathway reinvigorates exhausted CD8(+) T cells, it fails to restore T cell repertoire diversity

163 Quiescence is a hallmark of CD4(+) T cells latently infected with human immunodeficiency vi

164 The human T-cell leukaemia virus type 1 (HTLV-1) subtype c is ende

165 ifarnib as a potential therapeutic option in T-cell leukemia and TCL.

166 ed primary intestinal intraepithelial CD8(+) T-cell lines, or CD8(+) T cells directly isolated from i

167 f T-cell diseases, including some peripheral T-cell lymphomas, hemophagocytic lymphohistiocytosis, an

168 Tissue-resident memory (Trm) CD8(+) T cells mediate protective immunity in barrier tissues,

169 to determine whether Tregs suppress effector T cell-mediated and inflammatory cytokine-induced CEnC d

170 eir therapeutic activity in a mouse model of T cell-mediated autoimmunity that mimics multiple sclero

171 alization are important determinants of CD8+ T cell-mediated efficacy against SIV.

172 s not influence their ability to orchestrate T cell-mediated immunity.

173 A heterogeneous magnitude of CD4(+) T cell-mediated memory responses was observed in regard

174 NOD-scidIL2Rgamma(null) (NSG) mouse model of T-cell-mediated human islet allograft rejection and deve

175 We studied T cell memory in 42 patients following recovery from COV

176 not promote resurrection of exhausted CD4(+) T-cell memory in chronic infection.

177 in ligase Peli1 as an important regulator of T cell metabolism and antitumor immunity.

178 th enhanced cytolytic potential and requires T cell migration from lymph nodes for therapeutic effica

179 Although T cell migration is most frequently defined in the conte

180 lphabeta-TCR of mucosal associated invariant T cells, MR1 interacts with specific gammadelta-TCRs usi

181 Compared with conventional T cells, much less is known about the immune functions o

182 can be found in the peripheral blood CD4(+) T cells of patients at all stages of HIV-1 infection.

183 ic anti-CD19 chimeric antigen receptor (CAR) T cells offer a novel form of CAR-T-cell product that is

184 Enrichment of PD-1(+)CD4(+) T cells only within a granulocyte CN positively correlat

185 tration of DSS, transfer of CD4(+)CD45RB(hi) T cells, or infection with Citrobacter rodentium.

186 Cytotoxic T cells play a key role in adaptive immunity by killing

187 but instead are a broadly reactive layer of T cells poised to quickly develop into regulatory or eff

188 ntiation programs in the human CD8(+) memory T cell pool, with potentially broad implications for the

189 Additionally, vaccine-induced CD8 T cells poorly cross-recognized variant epitopes encodin

190 cells align closely with conventional memory T cell populations, bearing little resemblance to recent

191 e lymph nodes associated with differences in T cell populations.

192 CR) sequencing reveal lineage connections in T cell populations.

193 enance of extraordinarily large CMV-specific T cell populations.

194 ossible to visualize antigen-specific CD8(+) T-cell populations in vivo, which may serve prognostic a

195 ts an important role for B cells in indirect T cell priming and further emphasizes the advantage of c

196 ptor (CAR) T cells offer a novel form of CAR-T-cell product that is available for immediate clinical

197 discuss the innovative designs of novel CAR T cell products that are being developed to increase and

198 hat checkpoint inhibitor treatment increased T cell proliferation and functionality, but its influenc

199 ll antileishmanial drugs inhibit CD4 and CD8 T cell proliferation at the doses that are not related t

200 e exhibited much stronger Ag-specific CD4(+) T cell proliferation ex vivo.

201 We show here that AX-024 reduces T cell proliferation upon weak TCR stimulation but does

202 Cytokines that stimulate T cell proliferation, such as interleukin (IL)-15, have

203 lation between IVIG dose and toxin-triggered T-cell proliferation (r = -.67, P < .0001).

204 found that dual PARP-1/PARP-2-deficiency in T cells promotes tumor growth while single deficiency of

205 ave transformed cancer treatment by enabling T cell reactivation; however, response biomarkers are re

206 T cell reactivity against SARS-CoV-2 was observed in une

207 y, but its influence on the antigen-specific T cell receptor (TCR) repertoire is unknown.

208 Activation of the T cell receptor (TCR) results in binding of the adapter

209 Transcriptional profiling coupled with T cell receptor (TCR) sequencing reveal lineage connecti

210 Adoptively transferred T cell receptor (TCR)-transgenic T cells (TCR-T cells) a

211 T cell receptor sequence comparison between patients ide

212 matical modeling and statistical analyses of T cell receptor sequencing data, we develop a quantitati

213 fect phosphorylation of Zap70 (zeta chain of T cell receptor-associated protein kinase 70).

214 with a substantial increase in the number of T-cell receptor (TCR) sequences and their cognate antige

215 ng through multiple receptors, including the T-cell receptor (TCR), co-receptors, and cytokine recept

216 r and regulatory T-cell subsets with diverse T-cell receptor clonotypes in the periphery.

217 cocultured T cells expressing MCPyV-specific T cell receptors (TCRs) show increased cytokine producti

218 esting fundamental differences in gammadelta T cell recognition.

219 entially enhance our understanding of CD4(+) T cell recognition.

220 e PPE (Pro-Pro-Glu) proteins are targets for T-cell recognition in Mtb.

221 s could benefit from such products, since no T cells recognizing any EBV-derived peptide in this comm

222 in the central nervous system is crucial for T cell recruitment and reactivation into a pathogenic Th

223 cDC1s in expansion of tumor-specific CD8(+) T cells remains unclear.

224 xhausted CD8(+) T cells, it fails to restore T cell repertoire diversity.IMPORTANCE Checkpoint inhibi

225 gly shaped the circulating HCV-specific CD4+ T cell repertoire, suggesting antigen-independent surviv

226 onclusion, we show that MEKi leads to CD8(+) T cell reprogramming into T(SCM) that acts as a reservoi

227 response eQTLs (reQTLs) in myeloid cells and T cells, respectively.

228 NINJA will enable studies of how T cells respond to defined neoantigens in the context of

229 f H-2D(b) on CD11c(+) APCs mitigates the CD8 T cell response, preventing early viral clearance and im

230 ads to the development of a strong anti-ZIKV T-cell response without eliciting significant anti-ZIKV

231 iming and effector phases, provokes systemic T cell responses against dominant and subdominant neoant

232 cine was safe and elicited mutation-specific T cell responses against predicted neoepitopes not detec

233 rsus acute viral infections and identify CD8 T cell responses and downstream anorexia as driver mecha

234 d factors determining successful mounting of T cell responses are poorly defined.

235 Total and spike-specific T cell responses correlated with spike-specific antibody

236 demonstrated that SYIPSAEKI-specific CD8(+) T cell responses elicited by viral-vectored CSP-expressi

237 metabolic pathways that underly normal human T cell responses have taught us that there is still much

238 late and coordinate alphabeta and gammadelta T cell responses remains unknown.

239 pic model of TCR signaling in which multiple T cell responses share a common rate-limiting threshold

240 SARS-CoV-2-specific T cell responses were driven by TCR clusters shared betw

241 ive range, multifunctional CD8(+) and CD4(+) T cell responses with S protein-specific killing activit

242 eptor programmed cell death 1 (PD1) inhibits T cell responses, and blockade of this interaction has p

243 nate immune responses and adaptive cytotoxic T cell responses.

244 icrobiome shifts and enhanced intestinal CD8 T cell responses.

245 elicit broadly protective CD4(+) and CD8(+) T cell responses.

246 cells and the induction of protective CD8(+) T cell responses.

247 ur findings indicate that poor LASV-specific T-cell responses and activation of nonspecific T cells w

248 el, Tregs are known to inhibit effector CD8+ T-cell responses and contribute to virus persistence.

249 sed to measure the frequency of EBV-specific T-cell responses between groups following stimulation wi

250 e development of both anti-ZIKV antibody and T-cell responses in C57BL/6 mice.

251 B*57:01-restricted, HIV epitope-specific CD8 T-cell responses showed beneficial functional patterns a

252 The Matrix-M1 adjuvant induced CD4+ T-cell responses that were biased toward a Th1 phenotype

253 Total memory T-cell responses were measured after anti-CD3 or vaccini

254 Ankara vector to induce HBV-specific B- and T-cell responses.

255 ive compared to PD-1 signaling; (2) PD-L1(+) T cells restrained effector T cells via the canonical PD

256 Finally, deletion of Dot1L in T cells resulted in an impaired immune response.

257 f STAT1 signaling, however, depletion of CD8 T cells resulted in lytic infection of the choroid plexu

258 Loss of Yap in T cells results in enhanced T-cell activation, different

259 iated with potent antiviral function: memory T cells secreted cytokines and expanded upon antigen re-

260 me, phenotype, and function of memory CD8(+) T cells, sharing the same HSV-1 epitope-specificities, f

261 Using G9Calpha(-/-)CD8(+) T cells specific for proinsulin, we studied the mechanis

262 sing macrophage-specific (CD14) but not CD4+ T cell-specific (CD3) antibodies, suggesting that M-trop

263 A distinct TEMRA CD8(+) T cell subpopulation was identified that was characteriz

264 of VISTA disrupted the major quiescent naive T cell subset and enhanced self-reactivity.

265 The discovery of CD4(+) T cell subset-defining master transcription factors and

266 esence of functional effector and regulatory T-cell subsets with diverse T-cell receptor clonotypes i

267 -cell depletion, impacting both conventional T cells (T(conv)) and T(regs), subsequently followed by

268 These drawbacks can be circumvented by CAR-T cells targeting tumour-specific driver gene mutations,

269 transferred T cell receptor (TCR)-transgenic T cells (TCR-T cells) are not restricted by cell surface

270 elimination of a reservoir of infected CD4+ T cells that persists despite HIV-specific cytotoxic T c

271 Human skin contains a population of memory T cells that supports tissue homeostasis and provides pr

272 ) or derived from mature conventional CD4(+) T cells that underwent TGF-beta-mediated conversion in t

273 In support, adoptive transfer of old CD4(+) T cells that were transfected with a lentiviral vector i

274 The application of adoptive T cell therapies, including those using chimeric antigen

275 imeric antigen receptor-modified T-cell (CAR-T-cell) therapy are limited.

276 ncreased HIV-1 replication in primary CD4(+) T cells, thereby suggesting that Tim-3 expression might

277 etion of circulating and perivascular memory T cells, this brain signature was enriched and the surve

278 ced proliferation of naive CD4(+) and CD8(+) T cells to a larger extent than B. burgdorferi.

279 us and influences the susceptibility of CD4+ T cells to HIV-1 replication.

280 ranslates in vivo to an improved ability for T cells to infiltrate and repress tumors.

281 These TCR/CD3 bispecifics can redirect T cells to kill tumor cells with target HLA/peptide on t

282 ved drug FTY720 increased the sensitivity of T cells to the cytokine interleukin-2 (IL-2) through a p

283 en-specific progeny of individual naive CD8+ T cells to the T effector (TEFF), T circulating memory (

284 ing chimeric antigen receptor (CAR)-modified T cells, to solid tumors requires combinatorial strategi

285 In tracking the journey of T cells traversing from the thymus to the periphery and

286 However, Batf3 (-/-) T cells underwent increased apoptosis during contraction

287 ng; (2) PD-L1(+) T cells restrained effector T cells via the canonical PD-L1-PD-1 axis and were suffi

288 The number of intravascular CD3+CD8+ T cells was influenced by CM status (CM+ > CM-, P = 0.00

289 ing the risk of progression using naive CD4+ T-cells was predictive of progression along the whole IA

290 pitopes targeted by clusters of Mtb-specific T cells, we carried out a screen of 3,724 distinct prote

291 T cells were sampled for up to 11 weeks to capture stead

292 Resting CMV-specific CD8 T cells were terminally differentiated and expressed hig

293 rized population of extrafollicular B helper T cells, which produced IL-10 and could play a prominent

294 ell killing by freshly isolated human CD8(+) T cells, which represent a challenging but valuable mode

295 overexpression promoted activation of CD4(+) T cells while suppressing CD5(+) B-1a cell development.

296 CD29 also marked T cells with cytotoxic gene expression from different ti

297 cell responses and activation of nonspecific T cells with homing capacity to inflamed tissues are ass

298 T(SCM) that acts as a reservoir for effector T cells with potent therapeutic characteristics.

299 ssible to defeat this mechanism and activate T cells with solution ligands by cross-linking pMHC or u

300 umor antigen- and oHSV antigen-specific CD8+ T cells within 7 days after oHSV injection.