ライフサイエンスコーパス: T-cell activation

1 vity reaction accompanied by enhanced CD4(+) T cell activation.

2 S-CoV-2 infection may be compromising CD8(+) T cell activation.

3 Cs) are antigen-presenting cells controlling T cell activation.

4 stiffness lowers the agonist dose needed for T cell activation.

5 ignals, a signal we refer to as signal 4 for T cell activation.

6 , providing mechanical cues that costimulate T cell activation.

7 nteractions with HLA-I and diminished CD8(+) T cell activation.

8 sphorylation and increased antigen-dependent T cell activation.

9 sters are essential for robust inhibition of T cell activation.

10 nes by the time-resolved data recorded after T cell activation.

11 ing that gene deletion occurs independent of T cell activation.

12 madelta T cells results in heightened CD4(+) T cell activation.

13 ontrol spatiotemporal gene expression during T cell activation.

14 ic changes of miRNA controlled networks upon T cell activation.

15 duction of dysfunction-associated genes upon T cell activation.

16 f IRAP-dependent endosomal TCR signalling in T cell activation.

17 ctin-9 was recruited to immune synapses upon T cell activation.

18 tivation genes, a process that mimics normal T cell activation.

19 Conversely, overexpression of MLK3 decreases T cell activation.

20 T cell priming, but also for initial CD4(+) T cell activation.

21 ector and memory cell differentiation during T cell activation.

22 nd present pathogen-derived peptides for CD4 T cell activation.

23 s multiple donors on a dynamic background of T cell activation.

24 effector functions, cytokine production, and T cell activation.

25 regulate the expression of genes involved in T cell activation.

26 promotes both Listeria infection and CD8(+) T cell activation.

27 eversing agent bryostatin without increasing T cell activation.

28 on and processing genes and, in turn, CD8(+) T cell activation.

29 to delay disease onset by blocking effector T cell activation.

30 on during blood clotting, bone formation and T cell activation.

31 -gamma1), an important effector molecule for T cell activation.

32 ternal-fetal interface and cervix induced by T cell activation.

33 ions, in the interfollicular zone, a site of T cell activation.

34 nteractions are necessary to stimulate early T cell activation.

35 l and alternative p38 pathways contribute to T cell activation.

36 etry provided a rapid means of assessing CAR-T cell activation.

37 uman CD4 cells demonstrated its influence on T cell activation.

38 he daytime of genes and pathways involved in T cell activation.

39 e dendritic cells and MHCII-dependent CD4(+) T cell activation.

40 d for responding to agonistic antigen-driven T cell activation.

41 coinhibitory molecules necessary for higher T cell activation.

42 ng capacity of DCs and tumor-specific CD8(+) T cell activation.

43 d CD80 is a costimulatory receptor promoting T cell activation.

44 osphorylation by Lck is an essential step in T cell activation.

45 he programme of signalling events leading to T cell activation.

46 ly decreased LRBA and CTLA-4 expression with T-cell activation.

47 ire miRNome over a period of 24 h upon human T-cell activation.

48 ration, migration, antigen presentation, and T-cell activation.

49 ed type I interferon signaling and cytotoxic T-cell activation.

50 blockade reduced both rosette formation and T-cell activation.

51 is revealed massive and escalating levels of T-cell activation.

52 nstrate its physiological role in regulating T-cell activation.

53 h pathogenic processes rely on CD28-mediated T-cell activation.

54 t to HVEM, UL144 only binds BTLA, inhibiting T-cell activation.

55 n II)-induced hypertension by limiting renal T-cell activation.

56 ariants with reduced HLA binding and reduced T-cell activation.

57 ical inflammasome activation and decrease in T-cell activation.

58 itory antigen-presenting cells that suppress T-cell activation.

59 eloid cells (IMC), leading to suppression of T-cell activation.

60 0 molecules/cell to 1600 molecules/cell upon T-cell activation.

61 ial fusion proteins that cause CD19-specific T-cell activation.

62 avir with HLA-B*57:01 binding and the CD8(+) T-cell activation.

63 n of graft rejection relies on inhibition of T-cell activation.

64 f rosetting, but almost completely abrogated T-cell activation.

65 alleles were associated with CD8 and/or CD4 T-cell activation.

66 Dipyridamole also reduced CD4+ T-cell activation (-11.11% change; P = .006) in the pool

67 There was a modest decrease in CD8+ T-cell activation (-17.53% change for dipyridamole vs +1

68 ibited significantly higher levels of CD4(+) T cell activation, a difference that was lost over the f

69 transgenic to follow the onset of autoimmune T cell activation after regulatory T cell depletion in a

70 In vivo T cell activation also induced B cell cytokine responses

71 (Ab)-stimulated CD4+ T cells led to enhanced T cell activation; also, IL-10 depletion with neutralizi

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

73 lso occurred; notably, an increase in CD8(+) T cell activation, an increase in myeloid cells in the b

74 suppresses HIV-1 transcription by inhibiting T cell activation and by modulating RNA splicing.

75 ributing to HIV-1 pathogenesis by triggering T cell activation and cell death during viral spread.

76 6 function contributes to Tfh/non-Tfh CD4(+) T cell activation and cellular susceptibility to HIV inf

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

78 ll clones (TCC) and characterize pathways of T cell activation and cross-reactivity with clozapine me

79 Finally, we show that T cell activation and cytokine responses are influenced

80 n of sirolimus significantly attenuated CD8+ T cell activation and decreased VEGF-A levels.

81 5 regulates multiple distinct checkpoints in T cell activation and differentiation and that these are

82 abolic reprogramming plays a central role in T cell activation and differentiation, and the inhibitio

83 driven by T cell signaling, promote effector T cell activation and expansion and Treg dysfunction.

84 r, the mechanisms by which iron controls CD4 T cell activation and expansion remain poorly understood

85 s expressed by T cells, therefore inhibiting T cell activation and function.

86 aling is emerging as a critical regulator of T cell activation and function.

87 tory cytokines are sufficient for memory CD8 T cell activation and gain of effector functions, indica

88 d endogenous PD-L1 expression and restricted T cell activation and graft rejection.

89 ating an environment that stimulates mucosal T cell activation and inflammatory Th cells.

90 species and to limiting superantigen-induced T cell activation and interferon gamma (IFN-gamma) produ

91 D-1H), a CD28/B7 family molecule, coinhibits T cell activation and is an attractive immunotherapeutic

92 is a hallmark of both early antigen-specific T cell activation and later chronic stimulation, suggest

93 domain in the T cell compartment reduced the T cell activation and maintained the expression of CD62L

94 ivation of AKT, a kinase that is pivotal for T cell activation and metabolism.

95 We describe distinct helper T cell activation and migration profiles along the colon

96 llular galectin-9 is a positive regulator of T cell activation and modulates the pathogenesis of auto

97 trast, persisting viremia continued to drive T cell activation and PD-1 and CTLA-4 expression, and bl

98 through alpha(4)beta(7) resulting in CD4(+) T cell activation and proliferation.

99 on of 15-keto PGE(2) suppressed conventional T cell activation and proliferation.

100 mulatory pathway had minimal effect on early T cell activation and proliferation.

101 fects disappeared during ART, greater CD4(+) T cell activation and reduced CD107a expression on CD8(+

102 phils from CVID patients actively suppressed T cell activation and release of IFN-gamma via the produ

103 rity of this compartment is also crucial for T cell activation and survival after suboptimal TCR acti

104 ing mice with anti-MerTK antibody stimulated T cell activation and synergized with anti-PD-1 or anti-

105 s of disease development include Ag-specific T cell activation and Th1 differentiation, followed by T

106 rance from the blood coincided with peak CD8 T cell activation and the appearance of KFDV-specific Ig

107 17beta-estradiol, which contributes both to T cell activation and to reduced viral replication.

108 ivated T cells (NFAT) has a key role in both T cell activation and tolerance and has emerged as an im

109 ced CD4 T cell counts and elevated levels of T cell activation and viral load; it also independently

110 totoxicity of GPRC5D+ cells with concomitant T-cell activation and also killed plasma cells in MM pat

111 s of T-cell phenotype, function, pathways of T-cell activation and cross-reactivity with structurally

112 e (ii) blinatumomab induced B-cell-dependent T-cell activation and cytokine release to potentially tr

113 recapitulated the patients' defective CD8(+) T-cell activation and cytotoxicity against EBV-infected

114 ol Ca2+ fluxes that are essential for mature T-cell activation and differentiation and protection fro

115 ntrol may be explained by an increase of CD8 T-cell activation and exhaustion before LoC.

116 nical Trials Group study A5308 found reduced T-cell activation and exhaustion in human immunodeficien

117 ization of expression of CD30 and markers of T-cell activation and exhaustion were performed along wi

118 globulin mucin domain-3 (sTIM-3) (markers of T-cell activation and exhaustion), and sCD14 and sCD163

119 for the use of PET tracers that can monitor T-cell activation and expansion with high specificity.

120 cells, CD8+ T cells and NK cells, excessive T-cell activation and high expression of T-cell inhibito

121 TAT-5 signalling, thereby enhancing both CAR T-cell activation and homing to CXCL9/10-expressing tumo

122 ART in HIV controllers reduces T-cell activation and improves markers of immune exhaust

123 , we had shown ADPGK to play a major role in T-cell activation and induction of Warburg effect.

124 is, the full range of mediators that inhibit T-cell activation and influence anti-tumor immunity is u

125 d that the JAK inhibitor ruxolitinib dampens T-cell activation and lessens inflammation in a model of

126 ow cytometry, combined with overall elevated T-cell activation and memory differentiation, suggesting

127 CD8 T-cell activation and memory expansion are linked to HIV

128 plasma HIV-1 (single copy assay), and higher T-cell activation and PD-1 expression in men compared wi

129 d 4-1BBL provides co-stimulatory signals for T-cell activation and proliferation.

130 lenge for cancer immunotherapy is sustaining T-cell activation and recruitment in immunosuppressive s

131 T-cell activation and severity of acute pancreatitis did

132 -producing T cells together with features of T-cell activation and systemic inflammation identified h

133 70 binding protein that negatively regulates T-cell activation and tumor immunity.

134 ciated Rasal1 as a new negative regulator of T-cell activation and tumor immunity.

135 gnizes CD19 on neoplastic cells and triggers T-cell activation and tumor killing.

136 to explore how antigen expression influences T-cell activation and tumour growth.

137 the tetraspanin CD151 as a unique marker of T-cell activation and, in extension, an indicator of ele

138 FGL1 inhibits antigen-specific T cell activation, and ablation of FGL1 in mice promotes

139 l entry into the CR through HEVs, suppressed T cell activation, and altered T cell differentiation to

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

141 onse to influenza A virus infection, reduces T cell activation, and exacerbates morbidity.

142 CR):CD3 complex is required for USSN-induced T cell activation, and that direct receptor complex-part

143 tocol for APC-ms synthesis and use for human T-cell activation, and discuss important considerations

144 gnificantly reduced neutrophil infiltration, T-cell activation, and disease severity in mice.

145 testinal fatty acid binding protein (IFABP), T-cell activation, and the inflammatory markers C-reacti

146 DT in mitochondrial respiration and WDFY4 in T cell activation-and also suggests novel components for

147 In the presence of co-stimulation-deficient T cell activation, anergy is a dominant hallmark that ma

148 potent adjuvants to induce antigen-specific T cell activation, antibody production, and anti-tumor i

149 kin-2 (IL-2) and IL-15 play pivotal roles in T cell activation, apoptosis, and survival, and are impl

150 ilayers revealed that whereas late stages of T cell activation are thought to be substrate-stiffness

151 3 phosphorylation and calcium flux following T cell activation are unaffected.

152 inase activity, and free Lck mediated higher T cell activation as compared to coreceptor-bound Lck.

153 es a self-cleaving RNA and is cleaved during T-cell activation as well as thermal and endoplasmic ret

154 HSK requires T cell activation, as in the absence of T cells there is

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

156 ncing, confocal microscopy and a cognate CD4 T cell activation assay.

157 res, and these mapped to cytokine signalling/T-cell activation-associated pathways, with upstream dri

158 napse (IS) is a superstructure formed during T cell activation at the zone of contact between T cells

159 This approach enabled visualization of T-cell activation at early stages of disease, prior to o

160 selectin should be considered a regulator of T-cell activation at sites of immune activity.

161 unrecognized molecule, SRSF1, in restraining T cell activation, averting the development of autoimmun

162 hymotryptic beta5i subunit of i-20S inhibits T cell activation, B cell proliferation, and dendritic c

163 condary endpoints were changes in markers of T-cell activation, bacterial translocation, inflammation

164 These findings reveal differences in T-cell activation between responders and nonresponders e

165 amma and IL-2 expression and secretion after T cell activation but did not affect proliferation or ac

166 coreceptors are both positive regulators of T cell activation, but CD28 less potently induces TCR-pr

167 or (PD-1) results in residual suppression of T cell activation, but is not inhibited by ligand-antago

168 uppression of Malat1 is a hallmark of CD4(+) T cell activation, but its complete deletion results in

169 Together, these findings reveal that T cell activation by a bispecific T cell engager leads t

170 T cell activation by dendritic cells (DCs) involves forc

171 PTPN22 inhibits T cell activation by dephosphorylating substrates involv

172 show that electrophilic compounds can impair T cell activation by distinct mechanisms involving the d

173 Splenic CD4 T cell activation by particulate antigens is increased i

174 lass II cell surface expression and impaired T cell activation by peptide-pulsed macrophages.

175 These EPS-induced macrophages also limit T cell activation by S. aureus superantigens, and EPS ab

176 t blockade of such molecules facilitates the T cells activation by the DC vaccine.

177 TGF-beta influences the trajectory of early T-cell activation by altering PI3K activity and PtdIns l

178 this synapse is fully assembled and leads to T-cell activation by enabling interaction between the T-

179 As inappropriate T cell activation can cause disease, T cell quiescence m

180 and CD86, suggesting that Ag processing and T cell activation capabilities are impaired.

181 hat prior to inducing preterm birth, in vivo T cell activation caused maternal hypothermia, bradycard

182 emory, naive, and T-bet-Eomes- subsets), CD8 T-cell activation (CD38 expression) and T-cell immunoglo

183 A subgroup of patients had T cell activation characteristic of acute viral infectio

184 rtially maintained by negative regulators of T-cell activation, cytotoxic T-lymphocyte-associated ant

185 n to enhance mRNA stability, was involved in T cell activation-dependent mRNA stabilization.

186 Ca(2+) concentration, which is essential for T cell activation, differentiation and effector function

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

188 Strong T cell activation drives exhaustion(9,10), which may be

189 f genes involved in antigen presentation and T cell activation during EAU.

190 to orthogonal challenges, including reduced T cell activation during viral or bacterial infection.

191 T-cell activation ex vivo triggered psoriasiform and typ

192 ly window of susceptibility for pathological T cell activation following hematopoietic transplantatio

193 while NKG7 also had a major impact on CD4(+) T cell activation following infection.

194 rst time that EFs significantly downregulate T cell activation following stimulation with antigen-act

195 rofound differences in viral load and CD4(+) T cell activation from the earliest time points in men a

196 g proinflammatory cytokines, and an elevated T cell activation gene signature.

197 d threonine sites within proteins regulating T cell activation, gene expression, and protein translat

198 pletion in T cells leads to de-repression of T cell activation genes, a process that mimics normal T

199 nd conventional immunosuppressants targeting T cell activation had limited effects on controlling rej

200 ferentiation and effector function following T cell activation has been extensively studied, little i

201 ch of what we know about the early stages of T cell activation has been obtained from studies of T ce

202 maging constructs that can determine whether T-cell activation has occurred and could be used in drug

203 However, ascertaining whether T-cell activation has occurred in vivo is difficult with

204 d subsequently perturbed Ag presentation and T cell activation, higher TLR-mediated innate immune gen

205 Our findings revealed that T cell activation hinges on rare, long-dwell time bindin

206 sheds light on the relationship between HLA, T-cell activation, immune control, and HIV pathogenesis.

207 Thus, it clarifies the molecular picture of T cell activation in immune response.

208 nant cardiac antigen triggering post-MI CD4+ T cell activation in mice.

209 austion pathways in nonresponding tumors and T cell activation in responding tumors.

210 receptor module (either CD8 or CD4) to drive T cell activation in response to pMHCI/II.

211 mens, we identified a mechanism whereby CD8+ T cell activation in response to programmed cell death 1

212 Exosomal PD-L1 from the tumor suppresses T cell activation in the draining lymph node.

213 ted cells in the LN paracortex, which led to T cell activation in the LN interior.

214 ined the impact of L-selectin proteolysis on T cell activation in virus-infected mice.

215 T cells displayed intact, or even enhanced, T cell activation in vitro as measured by proliferation

216 However, unlike in men, higher CD4(+) T cell activation in women was not associated with highe

217 enhanced T-cell proliferation, and restored T-cell activation in the presence of VISTA-expressing ca

218 tissue-resident DCs, promoting disruption of T-cell activation in vitro.

219 son's HLA type may play a role in modulating T-cell activation independent of viral load and sheds li

220 diated cytokine production and do not induce T cell activation, independent of disease activity and t

221 T cell activation induced major chromatin remodeling, wh

222 and 2-DG was efficacious in dampening mouse T cell activation-induced effector processes, relative t

223 T cell activation is a cornerstone in manufacturing of T

224 CD4 T cell activation is critical to the initiation of adapt

225 ll-based therapies, and precise control over T cell activation is important in the development of the

226 T cell activation is initiated by signaling molecules do

227 As T cell activation is required to produce Abs, we wondere

228 cells and its expression is upregulated upon T cell activation, its function in non-Treg cells remain

229 rapidly and transiently expressed following T cell activation, its role in the early stages of T cel

230 Non-T cell activation linker (NTAL) is a lipid raft-membrane

231 n Americans exhibited elevated expression of T-cell activation markers and higher plasma levels of IL

232 validate an approach using Mtb-specific CD4+T-cell activation markers in blood to discriminate PTB a

233 L cells, AT1413 bTCE induced upregulation of T-cell activation markers, cytokine release, and T-cell

234 pression is regulated independently of other T-cell activation markers.

235 anscription factors that negatively regulate T-cell activation, may play a role in adaptive immune hy

236 w that L-selectin cleavage does not regulate T cell activation measured by CD69 or TCR internalisatio

237 Furthermore, these early T cell activation metrics were predictive of GVHD onset

238 rleukin-6 or D-dimer levels, nor on monocyte/T-cell activation, mucosal integrity, or intestinal micr

239 and cellular markers of monocyte activation, T-cell activation, oxidized lipids, and gut integrity.

240 CR, CD25 and PD1, three major players of the T cell activation pathway.

241 skin and provocation testing, and to explore T-cell activation pathways.

242 We use MULTI-seq to track the dynamics of T-cell activation, perform a 96-plex perturbation experi

243 shown to substantially impact human primary T cell activation phenotypes.

244 rutinib, ibrutinib had inhibitory effects on T cell activation, probably because of ITK inhibition.

245 including microRNAs (miRNAs), coordinate the T cell activation process.

246 T cell activation, proliferation and chemotaxis pathways

247 vival at least partially through diminishing T cell activation, proliferation and trafficking.

248 ing by PKCtheta was required for TCR-induced T cell activation, proliferation, and T(H)2 cell differe

249 s assay provides in-vivo-relevant off-target T-cell-activation readout.

250 T-cell activation releases inositol 1,4,5-trisphosphate

251 , molecular underpinnings promoting aberrant T cell activation remain poorly understood.

252 cellular signaling pathways that lead to CAR T cell activation remain unclear.

253 signaling apparatus, a process termed early T-cell activation, remains largely a mystery.

254 T-cell activation requires stimulation of specific intra

255 le and HLA-DR defining midterm and long-term T-cell activation, respectively, within skin-homing/cuta

256 TNIK-deficiency during T cell activation results in enhanced differentiation to

257 Quantitative mass spectrometry applied to T cell activation reveal key insights into signal transd

258 n, wound healing, and negative regulation of T-cell activation showed a significant dysregulation in

259 complex because of induction of the primary T cell activation signal.

260 Finally, T cell activation signature was detected at 1 K cell inp

261 extracellular adenosine levels and decreased T-cell activation significantly among persons with HIV-1

262 tral role, the basis for pox-specific CD4(+) T cell activation, specifically the origin of the poxvir

263 For example, specific glycans regulate T-cell activation, structures, and functions of immunogl

264 g to the antigen presenting protein CD1b and T cell activation studies are used to confirm the antige

265 tency of these compounds in inhibiting human T cell activation suggests that they may have therapeuti

266 By contrast, female patients had more robust T cell activation than male patients during SARS-CoV-2 i

267 L had higher CD4+ counts and lower levels of T-cell activation than those with detectable residual vi

268 costimulator (ICOS) is a specific marker of T-cell activation that can be imaged by radiolabeling an

269 ester (CFSE) release assay and evaluated CAR-T cell activation through interferon gamma (IFN-gamma) p

270 signaling complex and mediates inhibition of T cell activation through its association with Sts-2.

271 tential safety risk by triggering off-target T-cell activation through bivalent engagement and dimeri

272 ys (QVOAs) in which latency is reversed with T cell activation to allow viral outgrowth.

273 d detailed characterization of CAR-T and CCR-T cell activation to better understand their functional

274 nd ITK inhibitor, and administered it before T cell activation to direct differentiation toward a T s

275 e editing approaches beyond models of robust T cell activation to encompass both naive T cell homeost

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

277 MDR1 acted early after naive CD8+ T cell activation to suppress oxidative stress, enforce

278 kine levels; primary endpoints were cervical T cell activation, vaginal microbial diversity and cytok

279 e-associated protein 4 (CTLA-4), which limit T cell activation via synergistic mechanisms.

280 n how protein aggregates could induce DC and T cell activation via the FcgammaRIIa-Syk signaling path

281 , we investigated mechanisms for suppressing T-cell activation via the inhibitory receptor leukocyte-

282 V-domain immunoglobulin (Ig) suppressor of T cell activation (VISTA) is an immune checkpoint that m

283 munoglobulin domain-containing suppressor of T cell activation (VISTA) is expressed on naive T cells.

284 V-domain Ig suppressor of T-cell activation (VISTA) is an immune checkpoint that a

285 During ART, inflammation and CD4(+) T cell activation wane, resulting in reduced cell turnov

286 e found that when CMV was detectable, CD4(+) T cell activation was higher and CD8(+) T cell degranula

287 ng and anaphylactogenic potency but retained T-cell activation was generated.

288 While marked CD8 T-cell activation was observed with effector characteris

289 Following T-cell activation, WASP is degraded, leading to cytoskel

290 We show that IFN-I production and T cell activation were performed by the same pDC, but th

291 eutrophilia and higher levels of CD4 and CD8 T-cell activation were found in CDC patients as well as

292 be an important lever as they interfere with T-cell activation when activated by ICIs.

293 tion and epigenetic remodelling early during T cell activation, whereas complex II consumes the subst

294 gering sequential waves of polyclonal CD4(+) T cell activation while simultaneously enhancing virus p

295 f genes involved in antigen presentation and T-cell activation while repressing multidrug resistance

296 T and B cell infiltration and CD4+ and CD8+ T cell activation, while increasing Treg activation in p

297 ts at eight time points during memory CD4(+) T cell activation with high-depth RNA-seq in healthy ind

298 robial translocation (LPS, IFABP, sCD14, and T-cell activation), with decreased EndoCAb IgM.

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

300 secretion of costimulatory cytokines during T-cell activation, yet data to support this notion in vi