ライフサイエンスコーパス: restimulation

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

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

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

4 ame impaired ability to respond to antigenic restimulation.

5 tion, and IgM secretion upon subsequent TLR7 restimulation.

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

7 optive T cell therapy respond to melanoma Ag restimulation.

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

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

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

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

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

13 ased frequency and enhanced reactivity after restimulation.

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

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

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

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

18 toxic effector function, and the response to restimulation.

19 vitro assessment of cytokines after antigen restimulation.

20 -4 production upon polyclonal or Ag-specific restimulation.

21 responded rapidly and robustly to antigenic restimulation.

22 cells that are initially CLA negative before restimulation.

23 sitivity to Fas-mediated apoptosis after TCR restimulation.

24 and differentiate into effector cells on Ag restimulation.

25 ect the induction of hyporesponsiveness upon restimulation.

26 had a decreased proliferative response to Ag restimulation.

27 23p40 and IFN-gamma levels following ex vivo restimulation.

28 ry stimulation, but may become apparent upon restimulation.

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

30 gamma-inducible genes remained responsive to restimulation.

31 ogress through the cell cycle are anergic to restimulation.

32 nable to proliferate or to produce IL-2 upon restimulation.

33 effectors make less cytokines per cell upon restimulation.

34 production and proliferation in response to restimulation.

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

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

37 expression in dependence of T cell receptor restimulation.

38 -reacted with native proinsulin peptide upon restimulation.

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

40 % CI, 1.9-212; P = .004) after P. falciparum restimulation.

41 dy isotype controls MBC differentiation upon restimulation.

42 manner and maintains the Tr1 phenotype upon restimulation.

43 needed for TM cells to rapidly respond upon restimulation.

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

45 TH2 cytokine production upon peanut-specific restimulation.

46 witched secondary plasmablast responses upon restimulation.

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

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

49 racellular cytokine staining ex vivo without restimulation.

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

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

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

53 rofile in resting memory cells and following restimulation.

54 sponses when present only during alloantigen restimulation.

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

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

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

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

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

60 secreted gamma interferon following in vitro restimulation and demonstrated protection in the mouse t

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

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

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

64 promote tumor development by inhibiting CTL restimulation and expansion.

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

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

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

68 signaling, produce much less IFN-gamma upon restimulation, and are deficient in activation-induced c

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

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

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

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

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

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

75 Antigen-restimulation assays revealed that bp26 and TF stimulate

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

77 duced but did show cytokine production in Ag restimulation assays.

78 This property was recapitulated in in vitro restimulation assays.

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

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

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

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

83 tetramer treatment were rendered anergic to restimulation by antigen.

84 state, during which hMCP-1 was resistant to restimulation by either IFN-gamma or heterologous activa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 Upon restimulation, IL-2 transductants proliferated in the ab

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

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

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

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

126 T cells proliferated extensively to antigen restimulation in vitro and accumulated larger numbers of

127 measured by intact responses to alloantigen restimulation in vitro and in vivo.

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

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

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

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

132 posure to a tolerogenic stimulus in vivo and restimulation in vitro, wild-type T cells are blocked at

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 e production of interferon gamma after a 5-h restimulation in vitro.

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

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

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

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

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

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

144 Restimulation-induced cell death (RICD) regulates immune

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

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

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

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

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

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

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

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

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 on of P5 for 2 days were capable of in vitro restimulation of in vivo P5-primed T-cells (memory cells

167 e of ICOS/B7RP-1 interactions during ex vivo restimulation of lung Th2 effector cells prevented cytok

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

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

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

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

172 Restimulation of monocytes for DC maturation revealed th

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

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

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

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

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

178 In vitro restimulation of peripheral blood mononuclear cells from

179 Restimulation of peripheral T lymphocytes by inactivated

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

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

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

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

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

185 Restimulation of spleen and lymph node cells in vitro yi

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

187 In vitro restimulation of splenocytes by myelin oligodendrocyte g

188 n bacteriophage T4 Hsp10 have been mapped by restimulation of splenocytes from CBA/J and C57BL/6J mic

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

190 Restimulation of splenocytes with the corresponding immu

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

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

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

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

195 Restimulation of Th1 cells from LCMV-infected mice promo

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

197 Restimulation of the cells resulted in rapid eIF2alpha d

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

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

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

204 nd rendered them hyporesponsive to antigenic restimulation, resulting in 50--95% reduction of IL-4 an

205 In vivo restimulation revealed a greater impairment in the proli

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

207 Upon restimulation, T cells proliferated more vigorously and

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

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

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

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

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

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

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

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

216 Restimulation to detect low-frequency capsid-specific T

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

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

219 not alter the systemic immune response to Ag restimulation, unlike IL-4 immunoneutralization.

220 ration and cytokine production after antigen restimulation was assessed.

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

222 gamma and IL-12 release after Aspergillus Ag restimulation was elevated from spleen cells isolated fr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

244 duration of time that elapsed since the last restimulation with Ag.

245 duction of IL-4 and IFN-gamma secretion upon restimulation with Ag.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 Restimulation with individual peptides elicited distinct

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

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

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

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 contrast, restimulation with peptide D330N elicited cytokine profi

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

283 Restimulation with peptides W325A and V326A was also ass

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

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

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

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

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

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

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

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

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

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

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

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

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

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

298 Upon immunization and restimulation with tumors induced by the endogenous AKR/

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