ライフサイエンスコーパス: restimulation

1 ne-secreting T cell percentages upon antigen restimulation.

2 (+) T cells expressed low PRF levels without restimulation.

3 racellular cytokine staining ex vivo without restimulation.

4 roduction of IFN-gamma, IL-4, and IL-10 upon restimulation.

5 IL-10 and reduced IFN-gamma production upon restimulation.

6 zed phenotype both in vivo and after ex vivo restimulation.

7 rofile in resting memory cells and following restimulation.

8 sponses when present only during alloantigen restimulation.

9 ry cytokines IFN-gamma, IL-2, and IL-12 upon restimulation.

10 division and differentiation to ASC upon Ag restimulation.

11 ytokines on Nod2 or Toll-like receptor (TLR) restimulation.

12 neic T cells both in a primary MLR and after restimulation.

13 in an ameliorated response after subsequent restimulation.

14 ame impaired ability to respond to antigenic restimulation.

15 tion, and IgM secretion upon subsequent TLR7 restimulation.

16 ity of their progeny produced IFN-gamma upon restimulation.

17 optive T cell therapy respond to melanoma Ag restimulation.

18 urface and secreted TGF-beta1 and IL-10 upon restimulation.

19 following isolation, expansion, and antigen restimulation.

20 ls, increasing IL-4 and IL-10 secretion upon restimulation.

21 bly to that of control T cells on MOG(35-55) restimulation.

22 egulated IRAK-1 activation upon Nod2 or TLR4 restimulation.

23 f intracellular IFN-gamma and TNF-alpha upon restimulation.

24 signaling and unresponsiveness to antigenic restimulation.

25 ased frequency and enhanced reactivity after restimulation.

26 ls (LAT) is hypophosphorylated upon CD3/CD28 restimulation.

27 ed less IFN-gamma and more IL-2 upon in vivo restimulation.

28 levels of IL-10, but not IL-4, upon in vitro restimulation.

29 nt to apoptosis induced by Fas, TNF, and TCR restimulation.

30 toxic effector function, and the response to restimulation.

31 vitro assessment of cytokines after antigen restimulation.

32 -4 production upon polyclonal or Ag-specific restimulation.

33 responded rapidly and robustly to antigenic restimulation.

34 cells that are initially CLA negative before restimulation.

35 sitivity to Fas-mediated apoptosis after TCR restimulation.

36 and differentiate into effector cells on Ag restimulation.

37 ect the induction of hyporesponsiveness upon restimulation.

38 had a decreased proliferative response to Ag restimulation.

39 TH2 cytokine production upon peanut-specific restimulation.

40 ry stimulation, but may become apparent upon restimulation.

41 sion of IFN-gamma and TNF-alpha upon ex vivo restimulation.

42 gamma-inducible genes remained responsive to restimulation.

43 23p40 and IFN-gamma levels following ex vivo restimulation.

44 red with Seahorse technology on day 6 before restimulation.

45 s rapidly recruited to the LT/TNF locus upon restimulation.

46 D8(+) effector responses to tetramer-peptide restimulation.

47 expression in dependence of T cell receptor restimulation.

48 -reacted with native proinsulin peptide upon restimulation.

49 ed core 2 O-glycans independently of antigen restimulation.

50 % CI, 1.9-212; P = .004) after P. falciparum restimulation.

51 dy isotype controls MBC differentiation upon restimulation.

52 manner and maintains the Tr1 phenotype upon restimulation.

53 needed for TM cells to rapidly respond upon restimulation.

54 ot secrete IFN-gamma or IL-2 after antigenic restimulation.

55 witched secondary plasmablast responses upon restimulation.

56 that induced NKT cell anergy to alpha-GalCer restimulation.

57 but we found impaired responses to IFN-gamma restimulation.

58 ngly resistant to cell death by in vitro TCR restimulation, a finding that was recapitulated in Stat5

59 uce c-Jun/AP-1 expression on T cell receptor restimulation, a mechanism that may contribute to termin

60 cally resistant to apoptosis mediated by TCR restimulation, a process that normally constrains T cell

61 nduction of proapoptotic Fas ligand upon TCR restimulation, accounting for enhanced RICD sensitivity

62 Upon TCR restimulation, activated, cycling T cells can undergo a

63 ntenance of a subset that can be recalled by restimulation, analogous to T-cell effector cell and mem

64 essing the B-Raf transgene proliferated upon restimulation and displayed elevated ERK activation.

65 ced lower amounts of effector cytokines upon restimulation and displayed reduced proliferation compar

66 capable of IFN-gamma production upon peptide restimulation and expanded in response to challenge infe

67 promote tumor development by inhibiting CTL restimulation and expansion.

68 tivity that can be detected without in vitro restimulation and involves a T cell-specific (PI 3-kinas

69 DN T cells retained a stable phenotype after restimulation and that furthermore, the disappearance of

70 absence of Th induce TRAIL expression after restimulation and undergo activation-induced cell death.

71 reted interferon-gamma, expressed CD107 upon restimulation, and efficiently lysed HBV antigen-express

72 wing specific priming and secondary in vitro restimulation, antiretroviral CD8(+) CTL were identified

73 Therefore, at least two cycles of in vivo restimulation are needed for selection and expansion of

74 Antigen-specific ex vivo restimulation assays and in vivo killing assays demonstr

75 -induced T cell response was corroborated in restimulation assays by the observation that Ag-expanded

76 In vitro T cell restimulation assays demonstrated induction of a populat

77 le as a mechanism for this unresponsiveness, restimulation assays revealed increased production of re

78 Antigen-restimulation assays revealed that bp26 and TF stimulate

79 matically mapped in CBA/J and BALB/c mice by restimulation assays using a set of overlapping peptides

80 This property was recapitulated in in vitro restimulation assays.

81 rther, adding IL-13 at the time of Th17 cell restimulation attenuated IL-17A expression.

82 rate and produce IFN-gamma upon alpha-GalCer restimulation but retained the capacity to produce IL-4.

83 as cytotoxicity and cytokine secretion upon restimulation, but do not undergo a second round of clon

84 fferentiation of central-memory T cells upon restimulation by antigen within the CNS.

85 tetramer treatment were rendered anergic to restimulation by antigen.

86 e, CD8(+) T cells was independent of in vivo restimulation by MHC class I-expressing APCs.

87 nM treatment, HUVEC become refractory to the restimulation by OnM, measured as failure to reinduce SO

88 ed in this way could respond vigorously upon restimulation by producing increased IL-2 and proinflamm

89 m secondary lymphoid organs responded to TCR restimulation by proliferating, whereas T cells from the

90 Although unresponsive to restimulation by TCR/CD28 alone, restimulation with TCR/

91 ain access to Ag in peripheral tissues where restimulation can lead to activation-induced cell death

92 ased cytotoxicity of DPP1(-/-) CTL following restimulation coincided with increased expression of gra

93 yed enhanced innate cytokine production upon restimulation compared with PBMCs from controls, a diffe

94 owed poor IFN-gamma and IL-2 production upon restimulation, consistent with T cell anergy and similar

95 (+)) resided in BM in resting state but upon restimulation converted to IL-17/IFN-gamma-expressing ef

96 tion on sequential days to the antiviral CTL restimulation cultures of either 1) AKR.H-2(b) veto cell

97 /regulation of various cytokines in in vitro restimulation cultures were analyzed by enzyme-linked im

98 ines upon pattern recognition receptor (PRR) restimulation; cytokine attenuation to PRR stimulation i

99 large amounts of interferon (IFN)-gamma upon restimulation, DC2-primed CD8 T cells produced significa

100 ry cytokine and mediator expression upon TLR restimulation, demonstrating that LTbetaR signaling is i

101 Furthermore, we find that CD8 TRM-cell restimulation depends on a population of CD301b(+) antig

102 (-/-) Th2s failed to produce IL-4 protein on restimulation despite elevated IL-4/GATA3 mRNA.

103 for "immune antagonism" during memory T cell restimulation, despite observation of the latter at a mi

104 Following ex vivo restimulation, draining lymph node cells from misoprosto

105 fic CD8 T cells to secrete IL-2 on antigenic restimulation during primary infection were inversely co

106 ing anti-CD4(+) antibody during the in vitro restimulation ELISpot analysis failed to completely abol

107 these cells subsequently fail to divide upon restimulation, even in the presence of IL-2.

108 heir phenotype and functionality by means of restimulation ex vivo or antitumor efficacy in vivo.

109 After transfer and in vivo restimulation, gut or spleen memory cells proliferated,

110 This association increased after TCR restimulation in a SAP-dependent manner, requiring both

111 duction, and CTL lysis following Ag-specific restimulation in a vaccination setting.

112 allogeneic rapa-ECs became hyporesponsive to restimulation in an alloantigen-specific manner and cont

113 (DC) to CD4(+) T cell expansion in DLNs and restimulation in corneas is unknown.

114 direct role of viral latency and Ag-specific restimulation in driving the accumulation and maintenanc

115 centripetal pathway of migration would allow restimulation in lymph nodes, thereby promoting immune s

116 a robust recall response upon donor antigen restimulation in mixed lymphocyte cultures ex vivo.

117 a membrane, an effect that was reversed upon restimulation in presynapses but not in neighboring axon

118 IL-8, and IL-1beta upon Nod2, TLR4, and TLR2 restimulation in primary human monocyte-derived macropha

119 lls, reduces total T cell proliferation upon restimulation in secondary cultures (an effect dependent

120 pathway also occurred upon antigen-specific restimulation in TCR-transduced TIL1383I T cells prepare

121 XP3 expression, but lost them upon secondary restimulation in the absence of differentiation factors,

122 rred stability of FOXP3 expression upon Treg restimulation in the absence of exogenous TGF-beta1.

123 1 was detected in Th9 cultures after a final restimulation in the absence of polarizing cytokines.

124 ergo a second round of clonal expansion upon restimulation in the absence of T-cell help.

125 ls, GATA-3 mRNA half-life is increased after restimulation in the human T cell line Jurkat, in human

126 ced significant levels of IFNgamma following restimulation in the presence of IL-12.

127 ophage colony-stimulating factor (GM-CSF) on restimulation in vitro, and local GM-CSF was critical fo

128 d did not synthesize IL-2 or IFN-gamma after restimulation in vitro, indicating that they were not re

129 Our results show that, upon 5-d restimulation in vitro, M. tuberculosis-specific CD4(+)

130 o sensitive to IL-2-mediated cell death upon restimulation in vitro, the loss of SL9 T cells was mini

131 are hyporesponsive to B-cell receptor (BCR) restimulation in vitro.

132 r interferon-gamma response to IRBP(161-180) restimulation in vitro.

133 ng myelin oligodendrocyte glycoprotein 35-55 restimulation in vitro.

134 ecreased production of interleukin (IL)-2 on restimulation in vitro.

135 rably to that of control T cells on MOG35-55 restimulation in vitro.

136 d gamma interferon by CD4 T cells upon their restimulation in vitro.

137 vement to a deeper state of anergy following restimulation in vivo in a second Ag-bearing host was al

138 Upon further restimulation in vivo, CD4 memory T cells that had been

139 Blocking the PD1 pathway during ex vivo VZV restimulation increased the CD4(+) and CD8(+) proliferat

140 kine withdrawal induced death (CWID) and TCR restimulation induced cell death (RICD).

141 ike Th1, Th17 cells were highly resistant to restimulation-induced apoptosis, a major pathway by whic

142 Restimulation-induced cell death (RICD) regulates immune

143 This process, termed restimulation-induced cell death (RICD), is a mechanism

144 signal to achieve the threshold required for restimulation-induced cell death (RICD).

145 a self-regulatory form of apoptosis known as restimulation-induced cell death (RICD).

146 Mechanistic investigations revealed restimulation-induced cell death mediated by BIM and FAS

147 pon Ag exposure, most memory T cells undergo restimulation-induced cell death.

148 of memory human CD8(+) T cells with minimal restimulation-induced cell death.

149 to the relative resistance of Th17 cells to restimulation-induced cell death.

150 ses Rac1 and Rac2 as essential components in restimulation-induced cell death.

151 ent study, we chose IFN-gamma plus TNF-alpha restimulation-induced iNOS expression as a model of MSC

152 Understanding the control of Ag restimulation-induced T cell death (RICD), especially in

153 D8(+) T cell responses to persistent antigen restimulation is critical.

154 G vaccination enhanced cytokine responses to restimulation, it reduced systemic inflammation.

155 ate of cell refractoriness to subsequent LPS restimulation, known as endotoxin tolerance.

156 nses to varicella-zoster virus (VZV) ex vivo restimulation measured by responder cell-frequency and f

157 However, in a given restimulation, not all Th cells with a memory for IL-4 e

158 Furthermore, under serum-restimulation, nuclear translocation of both PGP9.5 and

159 Here we show that TCR restimulation of activated human CD4(+) T cells resulted

160 detrimental to both the priming and in vivo restimulation of Ag-experienced T cells.

161 ting autologous reactions (GvH): (1) optimal restimulation of autologous responder cells in secondary

162 lted in decreased levels of IFN-gamma during restimulation of B. burgdorferi-specific T cells in resp

163 ming growth factor beta (TGF-beta) inhibited restimulation of CTLs in PBLs with adenosine at IFNG bas

164 Upon restimulation of effector cells, IL-2 secretion and to a

165 In vitro restimulation of human CD8(+) T cells from a prostate ca

166 the inhibitory cytokine IL-10 during antigen restimulation of lymphocytes in vitro.

167 However, restimulation of MC with either PgLPS or EcLPS downregul

168 r the generation of Th1 immunity and for the restimulation of memory Th1 cells during secondary viral

169 Furthermore, in vivo Ag restimulation of MHC-II(-) memory B cells of IA-B mice f

170 Restimulation of monocytes for DC maturation revealed th

171 The restimulation of MP1xCD19 dual-specific CTLs in vivo by

172 representing an essential step for the local restimulation of myelin-specific T cells and the develop

173 We show that restimulation of neurons that were activated during a pr

174 production and degranulation responses after restimulation of PBMCs with inactivated rabies virus in

175 erferon-gamma were detectable after in vitro restimulation of PBMCs, and restricted epitopes were ide

176 Immune responses were assessed by in vitro restimulation of peripheral blood mononuclear cells and

177 In vitro restimulation of peripheral blood mononuclear cells from

178 Restimulation of peripheral T lymphocytes by inactivated

179 immune system priming against tumor Ags via restimulation of pre-existing (memory) antitumoral helpe

180 sequential recruitment of naive B cells and restimulation of previously recruited memory B cells.

181 ssion of Nab2 prevents TRAIL induction after restimulation of primary helpless CD8(+) T cells, and ex

182 Activation of DeltaMEKK3:ER* during serum restimulation of quiescent cells causes a strong activat

183 al replication ceased, but resumed following restimulation of rested cells with Ag or mAbs directed t

184 Restimulation of spleen and lymph node cells in vitro yi

185 GFP-specific restimulation of spleen cells from R. typhi(GFPuv)-infec

186 In vitro restimulation of splenocytes by myelin oligodendrocyte g

187 Restimulation of splenocytes with the Abeta1-15:DT conju

188 Restimulation of splenocytes with the corresponding immu

189 CII restimulation of T cells from CII/CFA-immunized mice res

190 Ex vivo restimulation of T cells showed decreases in IL-4, IL-5,

191 e a more robust antitumor immune response by restimulation of T cells with the E75 peptide vaccine, t

192 Furthermore, restimulation of T27K-primed PBMC with Ag-pulsed DCs gen

193 Restimulation of Th1 cells from LCMV-infected mice promo

194 However, such restimulation of Th1-primed cells from interferon (IFN)-

195 Restimulation of the cells resulted in rapid eIF2alpha d

196 of the persistence and the requirements for restimulation of the cytotoxic mediators granzyme B (GrB

197 After restimulation of their antigen receptor (TCR) by B cells

198 Restimulation of Thpp-like CD73+ Ly-6A/E- cells in Th1-

199 Restimulation of Tregs after 8-12 days of culture with C

200 Upon antigen restimulation of Vdelta2 T cells expanded in vitro in th

201 pecies and susceptibility to T-cell receptor restimulation or oxidation-mediated cell death.

202 secretion than B7-DC(-/-) DCs during T cell restimulation, possibly because they also express less B

203 on with improved responsiveness to antigenic restimulation post-REP.

204 B cells and show a faster and more vigorous restimulation potential, a hallmark of immune memory.

205 and perform conventional memory responses on restimulation: proliferation, migration and differentiat

206 In vivo restimulation revealed a greater impairment in the proli

207 A inhibition of granzyme C expression during restimulation significantly decreased cytotoxicity of DP

208 Upon restimulation, T cells proliferated more vigorously and

209 D2 stimulation induces non-responsiveness to restimulation, termed NOD2-induced tolerance.

210 O mice produced less IFN-gamma upon in vitro restimulation than Vbeta8(+) CD8 T cells from wild-type

211 tigen challenge of TNP-ovalbumin followed by restimulation, the Matk/CHK(-/-) lymph node and spleen c

212 on of GRAIL, a marker of T cell anergy; upon restimulation, these T cells showed reduced ability to p

213 effector T(H)1 cells, they proliferated upon restimulation, they exhibited cross-reactivity to some b

214 wing primary stimulation; however, following restimulation, they rapidly develop nonresponsiveness an

215 cells undergo rapid apoptosis in vitro upon restimulation through the TCR.

216 Ras/MAPK and NF-kappaB activity upon ex vivo restimulation through the TCR.

217 Restimulation to detect low-frequency capsid-specific T

218 However, on CD55 restimulation, Tr1s proliferated and maintained their di

219 In activated CD4(+) T cells, TCR restimulation triggers apoptosis that depends on interac

220 ration and cytokine production after antigen restimulation was assessed.

221 The hyporesponsiveness to TLR7 restimulation was associated with reduced NF-kappaB and

222 Hyporesponsiveness to restimulation was not due to apoptosis, generation of Fo

223 In vitro restimulation was not required for suppression by FV-ind

224 Killing mediated by DPP1(-/-) CTL following restimulation was rapid, perforin dependent, Fas indepen

225 ct of epigenetic silencing and of lymphocyte restimulation was studied.

226 hin lymph nodes, which is reduced by antigen restimulation, was critical for both viral control in ly

227 d shortly after vaccination, without ex vivo restimulation, was different among vaccine groups, sugge

228 ver, when CD8-independent T cell priming and restimulation were supplemented with IL-21, Ag-specific

229 cific CD4(+) T cells were less responsive to restimulation when initially stimulated by autologous li

230 erleukin 10 and interleukin 13 upon in vitro restimulation, which are also dampened in recipients tre

231 y state without need for exogenous antigenic restimulation, which is fundamentally different from tha

232 totoxic T lymphocytes (p-CTLs) compared with restimulation with (i) SIV Gag p55 alone or (ii) optimal

233 ionally tolerant in vivo, in that subsequent restimulation with a potent stimulus results in limited

234 D4+ T cell-mediated IFN-gamma after in vitro restimulation with A. phagocytophilum.

235 onse, whereas proliferation was absent after restimulation with Abeta1-15 or Abeta1-40/42 peptides, i

236 ccumulated T cells are profoundly anergic to restimulation with Ag in vitro.

237 olarity of the immune response upon in vitro restimulation with Ag is changed in wild-type mice, with

238 , cytokine expression was compared following restimulation with Ag vs agents that bypass TCR-proximal

239 to generate Th2 cell cytokines ex vivo after restimulation with Ag were also significantly reduced.

240 cells was maintained with IL-2, but not upon restimulation with Ag.

241 olytic function, but produced IFN-gamma upon restimulation with Ag.

242 h not anergic, are transiently refractory to restimulation with Ag.

243 f LAM also exhibited decreased response upon restimulation with Ag85B.

244 antation rapidly produce IFN-gamma following restimulation with alloantigen in vitro.

245 Upon restimulation with alpha-GalCer-pulsed CD1d(+) cells, ma

246 ssed proliferation of responder T cells upon restimulation with anti-CD3 mAb.

247 h node cells from immunized mice to in vitro restimulation with anti-CD3/CD28 antibody or autoantigen

248 Upon restimulation with anti-CD3/CD28 beads, the cultured Tre

249 Furthermore, following restimulation with anti-CD3/CD28, cytokine secretion by

250 ous lymphocyte-associated antigen, bypassing restimulation with antigen.

251 On restimulation with APC/peptide, the RTL-pretreated Th1 c

252 y measuring T-cell activation after in vitro restimulation with autologous tumor cells.

253 duction ex vivo by intracellular staining or restimulation with CII and enzyme-linked immunosorbent a

254 Following restimulation with DENV-infected dendritic cells, in viv

255 ere targeted by 45% to 74% of vaccinees upon restimulation with DNA-SMI-Gag matched peptides.

256 d interferon-gamma production in response to restimulation with donor alloantigen.

257 en, T lymphopenia, especially after in vitro restimulation with dual adjuvants, was observed, indicat

258 Following 3 days of restimulation with fresh allogeneic stimulators however,

259 nses, whereas proliferation was absent after restimulation with full-length Abeta or Abeta1-15.

260 y ligand PD-L1 and altered polarization upon restimulation with HBeAg.

261 on peripheral blood mononuclear cells after restimulation with heat-killed Mycobacterium tuberculosi

262 L-7, and IL-15 and rapidly proliferated upon restimulation with host dendritic cells.

263 est have enhanced IFN-gamma production after restimulation with IL-12 + IL-15, IL-12 + IL-18, or K562

264 Restimulation with individual peptides elicited distinct

265 Upon in vitro restimulation with infected antigen-presenting cells, CD

266 eas the GFP(-) TCR75 cells proliferated upon restimulation with K(d) peptide.

267 TNF-alpha), and interleukin-17 (IL-17) after restimulation with LcrV and YpL antigens.

268 After restimulation with lipopolysaccharide on day 6, (nor)adr

269 e secretion was measured after in vitro PBMC restimulation with low-dose IL-15, alone or in combinati

270 PS challenge, enterocytes become tolerant to restimulation with LPS or CpG DNA, but not with IL-17 or

271 -gamma and IL-17 secreted in vitro following restimulation with M. tuberculosis purified protein deri

272 Following in vitro restimulation with malaria-infected hepatocytes, CD11c(+

273 TIL infusion product, were hyporesponsive to restimulation with MART-1 peptide-pulsed dendritic cells

274 ior survival capacity and proliferated after restimulation with MART-1 peptide.

275 s defined by testing the reduced response to restimulation with mature dendritic cells generated from

276 These precursors yield, upon single restimulation with melanoma peptide-pulsed DCs, cytotoxi

277 zation during nonspecific activation or upon restimulation with mycobacterial antigens.

278 tory properties and FOXP3 demethylation upon restimulation with no stabilizing agent.

279 m RORgamma-deficient mice following in vitro restimulation with OVA compared with wild-type splenocyt

280 D8(+) cytotoxic T-lymphocyte responses, upon restimulation with OVA.

281 In vitro restimulation with P falciparum further increased IL-10

282 In contrast, restimulation with peptide D330N elicited cytokine profi

283 The cells were expanded by restimulation with peptides and demonstrated cytolytic a

284 Restimulation with peptides W325A and V326A was also ass

285 production and degranulation after in vitro restimulation with pertussis or H1N1 influenza vaccine A

286 n, however, was restored to normal levels by restimulation with phorbol myristate acetate (PMA)/ionom

287 Following in vitro restimulation with pMOG(35-55), splenocytes harvested fr

288 cit IFN-gamma, IL-5, or IL-13 secretion upon restimulation with Pn in vitro, whereas MyD88(-/-) mice

289 d from RPE cocultures were hyporesponsive to restimulation with splenic APC and Ag, but did not exhib

290 and PT32-challenged calves following ex vivo restimulation with T3SPs.

291 sponsive to restimulation by TCR/CD28 alone, restimulation with TCR/CD28 and either Stat4- or Stat6-m

292 ts S5A and S5G, which became apoptotic after restimulation with the inducer.

293 Low peptide concentration or restimulation with the parent peptide was used to enhanc

294 ntigen-specific T-cell hyporesponsiveness on restimulation with the recipient immunogenic DCs loaded

295 ession by these cells does not require their restimulation with the same allergen.

296 lation of CD69 did not become effectors upon restimulation with the same ligand and maintained an eff

297 kappaB activation and TNF-alpha release upon restimulation with the same LPS.

298 lymphocytes secreted interferon-gamma after restimulation with TSL or antigen 2/proline-rich antigen

299 es more comparable with those resulting from restimulation with wild-type peptide.

300 se to CMV exists in vivo than is revealed by restimulation with wild-type virus and adds to the evide