ライフサイエンスコーパス: T-cell activation

1 VISTA (V-domain Ig-containing Suppressor of T cell Activation).

2 ling, costimulatory pathways are involved in T cell activation.

3 riants with stronger suppression of in vitro T cell activation.

4 sent antigens, leading to systemic and local T cell activation.

5 ganization properties diminishes pAg-induced T cell activation.

6 he effect of CXCL4 in modulating DC-mediated T cell activation.

7 and kinase activity are induced upon CD4(+) T cell activation.

8 e that can clinically inhibit Vgamma9Vdelta2 T cell activation.

9 ts) on TCR-ligand interaction and subsequent T cell activation.

10 phase response as a result of Vgamma9Vdelta2 T cell activation.

11 y reconstruct regulatory networks underlying T cell activation.

12 een and liver, enhancing NK, NKT, and CD8(+) T cell activation.

13 on by the cells in which they are formed and T cell activation.

14 signaling pathways have been shown to impair T cell activation.

15 w the liver acts as a primary site of CD8(+) T cell activation.

16 identify the best cytokine producers during T cell activation.

17 RIg exacerbated islet inflammation and local T cell activation.

18 its expression was rapidly induced following T cell activation.

19 nces of collective bond behavior relevant to T cell activation.

20 structure has been shown to be important for T cell activation.

21 ide T cell receptor (TCR) ligation for naive T cell activation.

22 TAM phosphorylation, a crucial first step in T cell activation.

23 block upregulation of maturation markers or T cell activation.

24 tokine multiplex and naive autologous CD4(+) T cell activation.

25 timulatory molecule B7.2, and suppression of T cell activation.

26 results in sustained signaling and augmented T cell activation.

27 ntigen-presenting cells that are crucial for T cell activation.

28 n of OGT impaired nascent RNA synthesis upon T cell activation.

29 and APC contact zone, indicating its role in T cell activation.

30 e of the mechanisms used by MDSC to suppress T cell activation.

31 SH3.1-mutated Nck impaired TCR signaling and T cell activation.

32 vent of pAg sensing that ultimately leads to T cell activation.

33 on on regulatory or effector T cells reduces T cell activation.

34 g Th1 cell polarization and cytotoxic CD8(+) T cell activation.

35 piperacillin and the threshold required for T cell activation.

36 particularly those that depend on Ag-induced T cell activation.

37 -TCR stimulation and is required for optimal T cell activation.

38 ooperate and thus enhance the sensitivity of T cell activation.

39 T-1 even when stimulated by antigen-specific T cell activation.

40 haustion by regulating Pdcd1 expression upon T cell activation.

41 how downstream events can ultimately lead to T cell activation.

42 bacterial infections by controlling effector T cell activation.

43 e propose plays a crucial role in regulating T cell activation.

44 gt) is required for gastric colonization and T-cell activation.

45 presenting cells (APCs) and induce alphabeta T-cell activation.

46 o cross-present capsid antigen during CD8(+) T-cell activation.

47 d CD80 and CD86), is a negative regulator of T-cell activation.

48 ls, where it rapidly disassociated following T-cell activation.

49 eleton in regulating force generation during T-cell activation.

50 le measurement of MSC-mediated inhibition of T-cell activation.

51 LA-DR were used to define mid- and long-term T-cell activation.

52 associated with toxicity due to nonspecific T-cell activation.

53 by fluorescence in situ hybridization during T-cell activation.

54 h sources of unbiased data for understanding T-cell activation.

55 uences allergen uptake and allergen-specific T-cell activation.

56 protein kinase 70kDa (ZAP70) is required for T-cell activation.

57 ty and NFAT translocation, a measure of full T-cell activation.

58 les enriched in signatures reflecting higher T-cell activation.

59 rization, migration, and macrophage-mediated T-cell activation.

60 crophage antigen presentation and subsequent T-cell activation.

61 showed, in coculture, significantly reduced T-cell activation.

62 c-cell-specific program of regulatory CD4(+) T-cell activation.

63 ytokines and induced antigen-specific CD4(+) T-cell activation.

64 gen presentation, self-tolerance, and CD8(+) T-cell activation.

65 of Ca(2+) clearance in NFAT induction during T-cell activation.

66 2+) clearance regulates NFAT activity during T-cell activation.

67 all guanosine triphosphate protein linked to T-cell activation.

68 g its role as a novel regulator of naive CD4 T-cell activation.

69 t show how the mutations function to improve T-cell activation.

70 d, CD8+ T cells, and CD4/CD8 ratio) and CD4+ T-cell activation.

71 an attempted limitation of pathogenic CD8(+) T-cell activation.

72 For full T-cell activation, 2 signals must be received, and ligan

73 among antigen dispersal, DC positioning, and T cell activation after protein immunization.

74 tion, mononuclear phagocyte recruitment, and T cell activation, all of which are key steps in the con

75 T cell activation also led to changes in the relative ex

76 syndrome, which is characterized by massive T cell activation and a predominant Th1 profile of cytok

77 expression of genes that negatively modulate T cell activation and are associated with a hyporesponsi

78 vestigated their role in alloantigen-induced T cell activation and asked whether their absence might

79 Old mice accumulate defects in both CD8 T cell activation and cross-presentation.

80 tein SAP, probably as a result of continuous T cell activation and degradation by caspase-3.

81 Thus, defining unique aspects of CD4(+) T cell activation and development into Th1 effector cell

82 Costimulatory interactions are required for T cell activation and development of an effective immune

83 T) family are essential for antigen-specific T cell activation and differentiation.

84 in naive CD8(+) T cells plays a key role in T cell activation and differentiation.

85 fied a bystander mechanism that promotes CD8 T cell activation and expansion in untreated HIV-1-infec

86 ility complex class II, triggering a massive T cell activation and hence disease.

87 ling in adoptively transferred CTLs enhances T cell activation and IFN-gamma production in vitro, lea

88 r, these data indicate that LZTFL1 modulates T cell activation and IL-5 levels.

89 ntigen presentation thereby preventing early T cell activation and interferes with diapedesis.

90 ) is a coinhibitory receptor that suppresses T cell activation and is an important cancer immunothera

91 l in human T cell adaptogenomics that drives T cell activation and is required for signaling to cycli

92 ion of transcriptional programs that inhibit T cell activation and maintain tolerance.

93 and CD70, all of which are related to memory T cell activation and maintenance.

94 nd Runx3-activated ES-DCs exhibited enhanced T cell activation and migratory potential.

95 These pathways are essential for CD4(+) T cell activation and polarization, but little is known

96 Current immunosuppressive strategies inhibit T cell activation and prevent donor-recipient engagement

97 of Mer in dendritic cells promotes enhanced T cell activation and proinflammatory cytokine productio

98 ICOS regulates CD4(+) T cell activation and promotes the induction of follicul

99 hibited a dual function of attenuating early T cell activation and promoting the differentiation of F

100 ion in FMDV carriers suggested inhibition of T cell activation and promotion of Th2 polarization.

101 we analyze the contribution of PIP5Kbeta to T cell activation and show that CD28 induces the recruit

102 3 genes, T cell co-receptors/co-stimulators, T cell activation and signal-transduction genes.

103 important epigenetic modification during CD4 T cell activation and that JMJD3-driven H3K27 demethylat

104 The decision between T cell activation and tolerance is governed by the spati

105 portant for controlling the decision between T cell activation and tolerance via Cbl-b.

106 subtilis EPS can be used to broadly inhibit T cell activation and, thus, control T cell-mediated imm

107 presentation led to a clear reduction of DN T-cell activation and a decrease in the expression of in

108 timulates the CD27 pathway, which results in T-cell activation and antitumor activity in tumor models

109 g Administration-approved therapies, inhibit T-cell activation and cytokine production.

110 n significantly increased tumor-infiltrating T-cell activation and cytotoxicity and decreased the fre

111 ignaling and metabolic pathways critical for T-cell activation and differentiation into Th1 and Th17

112 their protein-coding target RNAs involved in T-cell activation and differentiation.

113 role for cyclin-dependent kinase 5 (Cdk5) in T-cell activation and effector function, but the contrib

114 tic cells (DCs), and is required for optimal T-cell activation and expansion.

115 eatment, expression of genes associated with T-cell activation and genes encoding inflammatory cytoki

116 nfected men and is associated with increased T-cell activation and HIV disease progression.

117 54-11.78) for the association between CD8(+) T-cell activation and infection with HIV-1.

118 As a consequence, CD4(+) T-cell activation and proliferation were also defective.

119 Furthermore, we observed pan-T-cell activation and redistribution from the circulatio

120 SC-derived macrophages were able to suppress T-cell activation and showed restored antimycobacterial

121 IL21 signalling pathway, in addition to CD4 T-cell activation and T-cell co-stimulation are critical

122 e T-cell receptor and STAT1, thus inhibiting T-cell activation and the antitumor immune response.

123 ents, (c) TCR signal transduction leading to T cell activation, and (d) TCR degradation.

124 ve increased germinal center (GC) responses, T cell activation, and AC accumulation within GCs.

125 he development of lymphadenopathy and CD4(+) T cell activation, and autoimmunity that mainly targeted

126 f inflammatory pathways: integrin signaling, T cell activation, and chemokine and cytokine signaling

127 e canonical domains for antigen recognition, T cell activation, and costimulation.

128 tric tissue T(reg) cells suppress endogenous T cell activation, and early T cell functionality is con

129 rete expression profiles during drug-induced T cell activation, and expression of each receptor was e

130 e MHC class I expression, impaired cytotoxic T cell activation, and poor patient prognosis.

131 mTOR, and mediators of endotoxin tolerance, T-cell activation, and viral defence.

132 I-induced hypertension, vascular injury, and T-cell activation; and gammadelta T cells are associated

133 s with biased capacity for CD4(+) and CD8(+) T cell activation are asymmetrically distributed in lymp

134 iscriminate self- and foreign antigen before T cell activation are unresolved.

135 Whereas metabolic changes occurring during T cell activation are well characterized, the metabolic

136 ets has illustrated that important facets of T-cell activation are controlled at the level of transla

137 ell receptor (TCR) triggering and subsequent T-cell activation are essential for the adaptive immune

138 e molecular mechanisms by which they control T-cell activation are incompletely defined.

139 to inhibit the unintentional Vgamma9Vdelta2 T cell activation as a consequence of aminobisphosphonat

140 tation genes, which correlated (r=0.78) with T-cell activation as measured by CD8-positive expression

141 iability but have increased inflammation and T-cell activation as they age.

142 that lymphostatin is likely to act early in T cell activation, as stimulation of T cells with concan

143 driven T cell proliferation in pDC-dependent T cell activation assays, but shifted cytokine productio

144 s of antibodies that block these pathways in T-cell activation assays.

145 measure the impedance change associated with T cell activation at electrical frequencies maximizing t

146 that were released from the periphery during T-cell activation became preferentially associated with

147 ily kinase Lck sets a critical threshold for T cell activation because it phosphorylates the TCR comp

148 ling cell constituents, and is essential for T cell activation, but its function in T cell polarizati

149 In addition, a restraint on T cell activation by CD6 was revealed in primary T cells

150 known to regulate effector versus regulatory T cell activation by DCs, selectively limits macropinocy

151 nvestigated whether type I IFNs regulate CD8 T cell activation by fungal beta-glucan particle-stimula

152 n of 76 kDa (SLP-76) plays a crucial role in T cell activation by linking antigen receptor (T cell re

153 atb1) restrains PD-1 expression induced upon T cell activation by recruiting a nucleosome remodeling

154 We investigated a mechanism for suppressing T cell activation by stimulating a natural inhibitory re

155 ify a new role for T cell TRAF3 in promoting T cell activation, by regulating localization and functi

156 there are conditions in which Vgamma9Vdelta2 T cell activation can be considered inappropriate for th

157 cine trial led to the hypothesis that CD4(+) T-cell activation can abrogate any potentially protectiv

158 This results in a reduced T cell activation capacity of DCs.

159 cytotoxicity response from a polyfunctional T cell activation caused hepatotoxicity and the rapid in

160 In vivo T-cell activation caused the TCR territories to contract

161 HCV-specific CD8 T-cell activation (CD107a, gamma interferon, macrophage

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

163 d markedly control DC-induced GAD65-specific T cell activation compared with poorly controlled patien

164 (+) cells specifically inhibited TH1 and CD8 T cell activation consistent with their co-localization

165 Our results identify distinct checkpoints of T-cell activation, controlling the capacity of myelin-sp

166 ty that titrating PD-1 expression during CD8 T cell activation could have important ramifications in

167 T-cell activation critically relies on the spatiotempora

168 the cell-associated HIV RNA level and CD4(+) T-cell activation decreased in the IFN group (n = 10).

169 es, and pathogenic infections can all affect T cell activation, differentiation, and the kinetics of

170 T cell activation drives proliferation but also reverses

171 s insight into the mechanisms underlying CD8 T cell activation during infection, which may be useful

172 own about their capacity to influence CD4(+) T-cell activation during a primary or secondary response

173 dendritic cell activity and by a decrease in T-cell activation, effects which are of importance durin

174 in T cells leads to aberrant and Th1-biased T cell activation, enhanced expression of integrin alpha

175 acellular signaling to impact the downstream T cell activation events.

176 okines simultaneously, as well as markers of T-cell activation, exhaustion, and maturation.

177 We analyzed plasma markers of inflammation; T-cell activation, exhaustion, proliferation; and innate

178 eater decline in CD8(+) compared with CD4(+) T cell activation, expansion, and clonal diversity.

179 pped LADs using Lamin B1-DamID during Jurkat T-cell activation, finding significant genome reorganiza

180 organs sustain the alloimmune response after T-cell activation has already occurred.

181 Once T-cell activation has occurred, however, stalling the re

182 netic landscape in response to Ag during CD4 T cell activation have not been well characterized.

183 ECM-resistant BALB/c mice leads to amplified T cell activation, higher serum gamma interferon (IFN-ga

184 ) are required for antigen receptor-mediated T-cell activation, how T-cells feedback to APCs to susta

185 The cell surface receptor CD6 regulates T cell activation in both activating and inhibitory mann

186 heral Th17 and Th22 cells and reduced CD4(+) T cell activation in gastrointestinal tissues post-FMT.

187 iotic treatment prevents pathological CD8(+) T cell activation in giardiasis.

188 e possible employment of impedance to assess T cell activation in label-free.

189 that, although distinct APCs initiate CD4(+) T cell activation in response to Ag expressed by intact

190 T cell activation in response to Ag is largely regulated

191 This may influence long-term T cell activation in response to TCR-CD3 stimulation.

192 ophage/T cell infiltration in the kidney and T cell activation in the renal draining lymph nodes.

193 not affect HIV-1 gene expression induced by T cell activation in these rCD4s.

194 R4-dependent manner, and these cells inhibit T cell activation in vitro and in C. rodentium-infected

195 nhibits vascular inflammation and suppresses T cell activation in vitro, we here tested the hypothesi

196 of these mechanisms as important in driving T cell activation in vivo.

197 IL-27R was shown to suppress T cells activation in atherosclerosis, however it's poss

198 antibodies can suppress autoreactive CD8(+) T-cell activation in a relatively selective manner.

199 T-cell recruitment, antigen acquisition, and T-cell activation in early vitiligo and reinforce the ro

200 the specific neoantigen qualities promoting T-cell activation in long-term survivors, we discovered

201 -induced SBP elevation, vascular injury, and T-cell activation in mice.

202 sessed based on helper T-cell and regulatory T-cell activation in mice.

203 ased CCR5 expression on T cells and dampened T-cell activation in peripheral blood without impairing

204 Allergen uptake and allergen-specific T-cell activation in relation to CD23 surface density we

205 assays, and the variant was found to silence T-cell activation in seven of the eight blood donors who

206 es strongly boosted antigen presentation and T-cell activation in the context of the human T1D suscep

207 e in nonatopic, nonallergic adults was muted T-cell activation in the peripheral blood and inflammato

208 Ang II-induced T-cell activation in the spleen and perivascular adipose

209 to DRbeta1-Arg74 could block the continuous T-cell activation in thyroiditis needed to maintain the

210 gocytose M. tuberculosis ex vivo and promote T-cell activation in vivo.

211 in A and lipid raft accumulation, as well as T cell activation, in a nonredundant manner.

212 The new macroencapsulation device abolished T cell activation induced by allogeneic splenocytes and

213 Importantly, T cell activation induces the expression of Hili in CD4(

214 ghts the importance of monitoring peripheral T cell activation inhibitor-mitochondrial expression, LB

215 Peripheral and intragraft expressions of T cell activation inhibitor-mitochondrial were stable in

216 Global T cell activation is a well-characterized means of induc

217 the presence of tumor specific neoepitopes, T cell activation is actively suppressed in PDAC.

218 T cell activation is an energy-demanding process fueled

219 nstrates that lipid antigen presentation for T cell activation is inhibited by lipophilic pollutants

220 Bone marrow T cell activation is nonspecific, IL-12-dependent, and i

221 Proper T cell activation is promoted by sustained calcium signa

222 ster of differentiation 1 (CD1) proteins for T cell activation is susceptible to lipophilic environme

223 histocompatibility complex (p/MHC) leads to T-cell activation is not yet fully understood.

224 ides within MHC during positive selection or T-cell activation is undefined.

225 ays a key role in mitochondrial function and T-cell activation, is associated with both IL-6 signalin

226 somal traffic in TCR signal transduction and T cell activation leading to IL-2 production.

227 First, peripheral blood CD4(+) and CD8(+) T-cell activation levels initially decreased in M- parti

228 gh the B7-CD28 costimulatory axis during CD8 T cell activation limits terminal differentiation and pr

229 inant target proteins UL83 or UL123, and the T-cell activation marker interferon-gamma (IFN-gamma).

230 To investigate whether the T-cell activation marker soluble CD27 (sCD27) measured i

231 ti-CD40/CpG treatment led to upregulation of T cell activation markers in draining lymph nodes.

232 chromatic flow cytometry was used to analyze T-cell activation markers (CD107, CD154, interleukin-2 [

233 RNA profiling also detected differences in T-cell activation markers (including HLA-DR) but, overal

234 of the TH2-polarizing cytokine IL-4 and the T-cell activation markers CD69 and CD62L.

235 T-cell activation may be a biomarker for elevated HIV-1

236 ear organization, and changes in LADs during T-cell activation may provide an important additional mo

237 hopenia-induced proliferation (LIP) leads to T cell activation, memory differentiation, tissue destru

238 antibody production, cytokine secretion, and T-cell activation; moreover, B cell misregulation is imp

239 spite maraviroc prophylaxis showed increased T-cell activation, naive T-cell skewing, and elevated se

240 long with 12 signatures tracking CD8 and CD4 T-cell activation, natural killer cells, and IFN activat

241 teroidal anti-inflammatory drugs (NSAIDs) on T-cell activation of the IL-4 pathway in aspirin-sensiti

242 The causes and impact of T-cell activation on disease risk should be considered w

243 ines, costimulatory molecule expression, and T-cell activation on L lactis G121 challenge.

244 hal VACV intranasal challenge, or defects of T cell activation or T cell homing to the site of inocul

245 Defects in T cell activation, particularly in the costimulation ste

246 Molecular intermediates in T-cell activation pathways are crucial targets for the t

247 e quantitative PCR detected mRNAs for CD8(+) T-cell activation (Perforin 1, Granzyme B).

248 Vgamma9Vdelta2 T cell activation plays an important role in antitumor a

249 ivity is observed under conditions where the T cell activation probability is low.

250 tion of the normal immunological synapse and T cell activation process by HIV to boost the activation

251 tudy examined whether HIV co-opts the normal T cell activation process through the so-called immunolo

252 Interestingly, unlike for T cell activation profiles, the extent of B cell activat

253 we show that type I IFNs support robust CD8 T cell activation (proliferation and IFN-gamma and granz

254 regulates expression of genes essential for T cell activation, proliferation, and function.

255 -cBiTE-mediated oncolysis resulted in robust T-cell activation, proliferation, and bystander cell-med

256 Similarly, T-cell activation, proliferation, and cytokine expressio

257 tic cells in vivo and in vitro, IVM impaired T-cell activation, proliferation, and cytokine productio

258 to mediate target-effector cell association, T-cell activation, proliferation, and receptor diversifi

259 n, this mechanism is not so critical for CD8 T cell activation (promotes IFN-gamma production but not

260 orylated CD6 cytoplasmic Y662 residue during T cell activation, providing an activating signal to T c

261 control of this immune suppression-resistant T-cell activation represents one of the key unmet needs

262 inomannan (LAM)-induced inhibition of CD4(+) T cell activation resulted in CD4(+) T cell anergy.

263 optotic signaling pathways, the noncytotoxic T cell activation showed extended proliferative, metabol

264 innate proinflammatory response or increased T cell activation/skewing display a more impaired behavi

265 an over-representation of genes relevant for T cell activation, such as CD40L, IRAK1, IRAK2, STAT1, a

266 thway, or the loss of negative regulators of T cell activation, such as the E3 ubiquitin ligase Cbl-b

267 nificantly increased viral reactivation upon T-cell activation, suggesting an important role of Naf1

268 A methyltransferase expressed robustly after T-cell activation that regulates plasticity of CD4(+) T-

269 eased presentation of tumor Ags and adaptive T cell activation; the latter could be further augmented

270 onses while maintaining low levels of CD4(+) T-cell activation to avoid the generation of target cell

271 al and morphological events occurring during T-cell activation to model force generation and to revea

272 sensitive to apoptosis but also accelerated T cell activation under phorbol 12-myristate 13-acetate/

273 and Ag display, is not sufficient to hinder T cell activation, underlining the robustness of the T c

274 in CpG sites belonging to genes that mediate T-cell activation, uniquely correlated with clinical act

275 red endocytic lipid antigen presentation for T cell activation upon benzo[a]pyrene exposure.

276 proliferation that were induced after potent T cell activation using alphaCD3/alphaCD28 antibodies.

277 oid dendritic cell, natural killer (NK), and T-cell activation using flow cytometry on baseline and a

278 that during homeostasis, FRCs also suppress T cell activation via producing high level of prostaglan

279 egies to expand myeloma-specific T cells and T-cell activation via PD-1/PD-L1 blockade are currently

280 V-domain Immunoglobulin Suppressor of T cell Activation (VISTA) is an inhibitory immune-checkp

281 t into secondary lymphoid organs nor initial T cell activation was affected by Dll1/4 loss.

282 T cell activation was again dependent on type I IFNs pro

283 Treg-mediated suppression of SMX-NO-induced T cell activation was investigated.

284 T cell activation was reduced with DMF treatment, especi

285 Local T-cell activation was confirmed by increased tumor infil

286 This T-cell activation was not indiscriminate because we obse

287 Because miR-181a has been described to alter T cell activation, we hypothesized that manipulation of

288 We demonstrate the persistence of T-cell activation well beyond viral clearance and detect

289 Several genes that oppose T cell activation were downregulated in asthma, suggesti

290 involved in glycolysis, gluconeogenesis, and T cell activation were unaffected.

291 2 heterodimers, which promoted superadditive T cell activation when both antigens were encountered co

292 t molecule that suppresses CD4(+) and CD8(+) T cell activation when expressed on antigen-presenting c

293 Recently, they have been implicated in T cell activation, where small numbers of antigenic rece

294 HSECs are known to modulate T-cell activation, which led us to investigate whether t

295 We found that acute T cell activation with anti-CD3 mAb induced stronger sma

296 underlying mechanisms by which MIA leads to T cell activation with increased IL-17a in the maternal

297 While HCV-specific CD8 T-cell activation with cytolytic and antiviral effects w

298 ion to unparalleled levels and avoids global T-cell activation within resting CD4+ T-cells.

299 ent PD-L1 may result from the high degree of T-cell activation within the highly immunogenic milieu o

300 We use this selectivity to inhibit T cell activation without affecting major functions of m