ライフサイエンスコーパス: cell response

1 ution of plasminogen was downstream of the T-cell response.

2 the timing, magnitude, and quality of the T cell response.

3 infection contribute significantly to its T cell response.

4 on, and induction of a Bet v 1-independent T-cell response.

5 ge of the ongoing follicular T cell and GC B cell response.

6 r T cell survival into an efficient CD4(+) T cell response.

7 nonical antigenic epitopes targeted by the T cell response.

8 nge and dominated in the subsequent CD8(+) T cell response.

9 rghei infection is dominated by a Vbeta8.1 T cell response.

10 The immunized mice also developed a robust T cell response.

11 te and adaptive immunity, promoting potent B cell responses.

12 on in absence of detectable PvCSP-specific T cell responses.

13 essential for the appropriate analysis of T cell responses.

14 alterations in basophil reactivity but not T-cell responses.

15 hibited, altering DC outputs and enhancing T-cell responses.

16 and the subsequent development of effector T cell responses.

17 sociated with reduced ex vivo HIV-specific T cell responses.

18 f alloantigen that drives CD8(+) cytotoxic T cell responses.

19 for anticancer therapy enhancing antitumor T cell responses.

20 y molecule playing a role in physiological B cell responses.

21 l weakness contributes to restraint of IgE B cell responses.

22 eristics of tolDCs and subsequent effector T cell responses.

23 n conventional Treg cells, IL-2 inhibits TFR cell responses.

24 ficant role in regulating antigen-specific T-cell responses.

25 lity and antigenic targets of ZIKV-induced B-cell responses.

26 binding, virus neutralizing antibody, and T-cell responses.

27 bolism and function to limit DC-stimulated T-cell responses.

28 e correlated with impaired effector CD8(+) T cell responses.

29 IRF-1 prior to induction of adaptive B and T cell responses.

30 death-1 (PD-1) is a negative regulator of T-cell responses.

31 ion involving IL-36R/MyD88-dependent IL-17 T cell responses.

32 s, and blunted PE-specific germinal center B cell responses.

33 mmunoregulatory checkpoints that attenuate T-cell responses.

34 cells can actively control autoaggressive T cell responses.

35 tivate them to prime tumor-specific CD8(+) T cell responses.

36 ion, in the absence of modulation of T- or B-cell responses.

37 checkpoint role in inhibiting inflammatory T cell responses.

38 de (ICB) therapies can unleash anti-tumour T-cell responses.

39 e mechanism of controlling proinflammatory T cell responses.

40 -)) mice were used as a model for enhanced B-cell responses.

41 key integrators of antibody and T follicular cell responses.

42 ason or vaccination to assess antibody and T-cell responses.

43 ociated with effective Gag-specific CD8(+) T-cell responses.

44 the MVAgp140 boost, increased peak CD4(+) T cell responses.

45 high permselectivity and strong allogeneic T cell responses.

46 ha-(1,3)-glucan-mediated DC activation and T-cell responses.

47 al vectors and is known to generate potent T cell responses.

48 reasing the risk for seeding of autoimmune B cell responses.

49 rated that it safely induced serologic and T-cell responses.

50 esenting cells support different stages of B cell responses.

51 izing cytokines and promotion of antitumor T cell responses.

52 aim for effective and balanced humoral and T cell responses.

53 e no longer able to stimulate adequate CD8 T cells responses.

54 The definition of CD4(+) T cell responses after live vaccination is important becau

55 ibition of human T cells show that maximal T-cell responses against autoantigen or repeated tetanus t

56 CD4 TEMRA cells and provides insights into T-cell responses against DENV and other viral pathogens.

57 Here, we found that MAIT cell responses against Escherichia coli and Candida albi

58 Effective T cell responses against invading pathogens require the co

59 herapy is highly effective at reactivating T-cell responses against melanoma, which is postulated to

60 with asymptomatic infection have exhibited T cell responses against specific HSV-2 antigens not obser

61 It precludes specific T-cell responses against strong antigens and we found very

62 CD8(+) T-cell responses against the AAV capsid protein can, howev

63 d pigs, where specific CD8(+) T and CD4(+) T-cell responses against the GOI-encoded antigen were obse

64 IgG and robust gamma interferon-secreting T cell responses against the proteins.

65 residual Tregs were able to control CD8(+) T-cell responses against the tumor.

66 The immune system can mount T cell responses against tumors; however, the antigen spec

67 broblasts possess the capacity to suppress T cell responses, although the molecular mechanisms of thi

68 own to confer a strong IAV-specific CD8(+) T-cell response and a strong cross-strain as well as cross

69 induced a protective VACV-specific CD8(+) T cell response and protected against a lethal VACV challe

70 nti- Pp IgG antibody nor in vitro anti- Pp T-cell response and resultant production of RANKL was affe

71 during vaccination impaired protective CD8 T cell responses and ablated sterile protection.

72 ssion in B cells substantially enhanced GC B cell responses and anti-Plasmodium Ab production.

73 -intrinsic IFN-gamma and T-bet suppress GC B cell responses and anti-Plasmodium humoral immunity.

74 y-to-implement research tool for measuring T cell responses and cellular metabolic changes in vitro.

75 accompanied by augmented antitumor T- and B-cell responses and decreased infiltration of immunosuppr

76 and magnitude of the total virus-specific T-cell responses and directly with plasma levels of molecu

77 RATIONALE: Diverse B cell responses and functions may be involved in atherosc

78 DC were superior in stimulating allogeneic T cell responses and in cross-presenting viral antigens to

79 DC microenvironment to control DC-induced T-cell responses and indicate that glucose is an important

80 rovar Typhimurium (S Typhimurium) inhibits T cell responses and mediates virulence.

81 y associated with hyperactive conventional T cell responses and poor Treg-mediated suppression.

82 death-1 (PD-1)-targeted therapies enhance T cell responses and show efficacy in multiple cancers, bu

83 e was associated with the induction of CD4 T cell responses and the epitope preferentially binds MHC

84 isms by which noninflammatory SF modulate Th cell responses and to determine the immunosuppressive ef

85 roaches to reverse these programs improved T cell responses and tumor control during ICB.

86 hat share cross-reactivity in antibody and T cell responses, and co-circulate in increasing numbers o

87 blished EsxA secretion, host specific EsxA T-cell responses, and increased strain virulence.

88 ng CD8(+) cells, low virus-specific CD4(+) T-cell responses, and low Env antibody titers.

89 inst GVHD by modulating alloreactive donor T-cell responses, and that CXCR3 signaling may be an impor

90 logy, stronger and persistent natural killer cell responses, and the extended induction of pro-inflam

91 36) developed a robust immunodominant CD8 T cell response apparently cross-reactive between a newly

92 have demonstrated that the kinetics of the B cell response are similar for all four FMDV serotypes te

93 pectratyping revealed that SMX-NO-specific T cell responses are controlled by public TCRs present in

94 8(+) gamma interferon (IFN-gamma)-positive T-cell responses are essential for reducing parasite burde

95 While early effector T cell responses are required for limiting parasitemia, th

96 s that the attributes of protective CD4(+) T cell responses are still elusive for human TB.

97 Tumor-specific T cell responses are strongly impaired in CNI-treated pati

98 MDSCs were suppressive of autologous T-cell responses as evidenced by reduced T-cell proliferat

99 tions have provided the most insight, with T cell responses as well as detailed antibody responses ha

100 e findings, we propose a model in which Treg cell responses at peripheral sites converge on those sel

101 d by K cells is improved, probably because K cell responses become less rectified.

102 esponses, especially their ability to help B cell responses, become compromised with aging.

103 rate that initiation of the Vgamma9Vdelta2 T cell response begins with sensing of pAg via the intrace

104 source and suppressed diabetogenic CD8(+) T-cell responses both directly and through an intermediary

105 (IL-2) promotes Foxp3(+) regulatory T (Treg) cell responses, but inhibits T follicular helper (TFH) c

106 is capable of mounting an antigen specific T cell response by efficiently stimulating antigen cross-p

107 CS1 in dendritic cells (DCs) would improve T cell responses by accentuating IFN-gamma-directed immune

108 Purpose Ipilimumab increases antitumor T-cell responses by binding to cytotoxic T-lymphocyte anti

109 resulted in suppression of virus-specific B cell responses by inhibiting proliferation of germinal c

110 These findings suggest that inhibition of B cell responses by rapamycin may play an important role i

111 This degeneracy of the cell response can be linked to the initial paths that th

112 of vaccines designed to induce protective T cell responses can be positively modulated with chemical

113 While effective CD8 T-cell responses can control viral replication in conjunct

114 ent virus that elicits different cytotoxic T cell responses characterized as acute resolving or infla

115 ring mast cell development as augmented mast cell responses could be recapitulated in wt mast cells d

116 We identified autophagy as a pivotal cell response determining the efficiency of AAVs intrace

117 and functionality of ex vivo HCV-specific T-cell responses did not increase following RG-101 injecti

118 (HA) which potentially enhance regulatory T cell response due to conservation with the human genome,

119 ortant for boosting optimal primary CD4(+) T cell response during NS4B-P38G vaccination.

120 y present an important target to modulate NK cell response during pulmonary inflammation.

121 cific inhibitor of mTOR, on B cell and CD4 T cell responses during acute infection with lymphocytic c

122 y differentially regulating B cell and CD4 T cell responses during acute viral infection and that rap

123 role for CD103(+) cDCs in antigen-specific T cell responses during subclinical viral myocarditis.

124 ey transcriptional determinant controlling T cell responses during transplantation.

125 oprotein (GP) and examined GP-specific CD4 T cell responses elicited by Ad5 vectors and compared them

126 We find that memory T cell responses elicited by prior infection with DENV or

127 Our data show that memory T cell responses elicited by prior infection with DENV rec

128 T-cell responses, epitope mapping and cross-reactivity to

129 Naive CD4 T cell responses, especially their ability to help B cell

130 Analyzing human innate-like T cell and NK cell responses following infection with Plasmodium has b

131 sults reveal novel regulatory roles in the B cell response for receptors that are typically proinflam

132 ypothesized that targeting extrafollicular B cell responses for activation would improve the speed an

133 are produced in the absence of identified T cell responses for each citrullinated protein.

134 and the change in HIV-1 Gag-specific CD8+ T cell responses from baseline to day 28 after infusion.

135 Mechanisms that elicit mucosal TH17 cell responses have been described, yet how these cells

136 y with traditional methods for determining T cell responses (i.e., [(3)H]thymidine incorporation and

137 echanisms of antibody production in memory B cell responses.IgE is an important mediator of protectiv

138 methods for the detection of drug-specific B-cell responses, (ii) characterize drug-specific IgG subt

139 ay be further impacted by increased CD4(+) T cell responses.IMPORTANCE Prior immune correlate analyse

140 rons, normalized TH1 and follicular T helper cell responses, improved TH17 differentiation, cured muc

141 We studied the long-term cross-reactive T-cell response in 14 trivalent LAIV-vaccinated children u

142 rally well controlled by the HCMV-specific T cell response in healthy people.

143 t to investigate heterogeneity in the CD8+ T cell response in humans and mice, and show that it is ac

144 ricted epitope to which there was a CD8(+) T cell response in mice immunized with our modified dendri

145 Although the effector T-cell response in patients with celiac disease has been w

146 antiviral cytokines and an impaired CD4(+) T cell response in peripheral organs.

147 cidate the kinetics of the effector CD8(+) T cell response in the liver following Plasmodium berghei

148 The magnitude of the K(d)M282-90 CD8(+) T cell response in TLR agonist-treated neonates could be b

149 We evaluated the CD8(+) T cell response in ZIKV-infected LysMCre(+)IFNAR(fl/fl) C5

150 n to the viral load of HIV-specific CD4(+) T cell responses in a cohort of untreated HIV clade C-infe

151 cination induced strong mE6 and mE7 CD8(+) T cell responses in all mice, although they were significa

152 roducing T cells and might thus impact the T-cell responses in asthma.

153 The observed B-cell responses in both venom immunotherapy-treated patie

154 LAIV boosts durable, cross-reactive T-cell responses in children and may have a clinically pro

155 lucidate the global landscape of antitumor T cell responses in complete regression of human papilloma

156 cell levels) were performed according to Th cell responses in gingival tissues.

157 re successful in the induction of NAbs and T cell responses in guinea pigs.

158 rmine if these inhibitory pathways prevent T-cell responses in HCCs and to find ways to restore their

159 analyse the HDM-derived protein targets of T cell responses in HDM-allergic individuals, and investig

160 pot assay to interrogate CD8(+) and CD4(+) T cell responses in healthy volunteers infected with rDEN2

161 Functional analysis of T-cell responses in HIV-infected individuals has indicated

162 t effective agents in controlling effector T-cell responses in humans.

163 ore effective in reducing graft associated T cell responses in liver-Tx than in BM-Tx.

164 We found superior and durable B-cell responses in macaques vaccinated with an occluded C

165 etramers in evaluating HIV-specific CD4(+) T cell responses in natural infections.IMPORTANCE Increasi

166 ncy of cytomegalovirus (CMV)-pp65-specific T-cell responses in peripheral blood mononuclear cells (PB

167 and IL-37 in regulating CD4(+) and CD8(+) T cell responses in S. stercoralis infection.

168 ssor cells (MDSCs) are major regulators of T cell responses in several pathological conditions.

169 Meromycolate fine structure influences T cell responses in TB-exposed individuals, and meromycola

170 ergic innervation-mediated suppression of NK cell responses in the brain involves RUNX3.

171 ppresses follicular helper T cell-mediated B cell responses in the germinal center reaction.

172 vel role of IL-22 in controlling antiviral T cell responses in the non-lymphoid and lymphoid organs d

173 nsformative in promotion of anti-tumor CD8 T-cell responses in the treatment of certain malignancies.

174 provide new ways to suppress pathological T-cell responses in transplantation or autoimmunity.

175 cribe the appearance of transgene-specific T-cell responses in two subjects that were part of the pha

176 Importantly, CD4(+) T cell responses in vaccinees were similar in magnitude an

177 s, and there is compelling evidence for iNKT cell responses in various types of sterile inflammation.

178 critically required for antigen-stimulated T-cell responses in vitro and in vivo.

179 hey exerted a potent suppression on CD8(+) T cell responses in vitro.

180 that induce strong peptide-specific CD8(+) T cell responses in vivo by incorporating an NKT cell-acti

181 ed MHC-class I:peptide complexes stimulate T cell responses in vivo, further emphasizing the need to

182 protein and host NKR-P1B/C alleles impact NK cell responses in vivo.

183 vivo and defective cross-priming of CD8(+) T cell responses in vivo.

184 n 18 kDa (TSPO), a marker of activated glial cell response, in a cohort of National Football League (

185 fective method to determine the quality of T cell responses induced by, for instance, T cell vaccines

186 The Chlamydia-specific CD4 T cell response is characterized by the production of IFN-

187 unique impact of TLR agonists on neonatal T cell responses is important to consider for RSV vaccines

188 anding of the effect of CpG-A and CpG-B on B cell responses is incomplete.

189 fic signaling complexes to regulate specific cell responses is limited.

190 terial superantigens trigger a polyclonal T -cell response leading to a potentially catastrophic "cyt

191 ins may differentially modulate the CD4(+) T-cell responses, leading to the generation of Th17 cells

192 te lymphoid cells (ILCs) regulate adaptive T cell responses led us to examine the regulatory potentia

193 ivotal roles in pro-inflammatory T helper 17 cell responses linked to autoimmune and inflammatory dis

194 In light of dampened CD8(+) T-cell responses, liver disease often manifests systemical

195 We assessed T-cell response markers as correlates of risk in the HIV V

196 ral therapy, suggesting that the adaptive NK cell response may be inversely related with the degree o

197 Detailed knowledge of the T cell response may further contribute to the identificati

198 The HCMV-specific T-cell response may have a role in the prevention of virus

199 op particularly efficient antiviral CD4(+) T cell responses mediated by shared high-affinity TCRs.

200 Since whole cell responses most often arise from the coordinated act

201 id not generate an excessive primary CD4 TFH cell response nor an enhanced alloantibody reaction.

202 ntigen presentation are driving the robust T cell response observed during an M. tuberculosis infecti

203 The exacerbated mast cell responses observed in the absence of Dnmt3a were re

204 ouse model for evaluating anti-ZIKV CD8(+) T cell responses of human relevance.

205 s intestinal T cell homeostasis and alters T cell responses of mice in different animal facilities.

206 ere strongly associated with H1N1-specific B cell responses postvaccination.

207 accination approaches eliciting strong CD4 T cell responses provide only weak protection from tubercu

208 effector and central memory CD4+ and CD8+ T-cell responses reactive to peptides corresponding to bot

209 decidua, the functional properties of this T cell response remain poorly defined.

210 ponses in preclinical models, particularly T cell responses, remain sparse.

211 array, and functional ability to stimulate T cell responses, requires autocrine C3a receptor and C5a

212 cytomegalovirus (CMV) can elicit a CD8(+) T cell response restricted by the human MHC-Ib molecule hu

213 B-cell responses result in clonal expansion, and can occur

214 d similar HIV-1-specific CD4(+) and CD8(+) T cell responses, similar levels of binding IgG antibodies

215 Here we show blood central memory CD4 T-cell responses specific to Mtb dormancy related (DosR) l

216 lls with nutrients and oxygen thus affecting cell responses such as motility.

217 During CD8(+) T cell responses, Tcf1 long isoforms were dispensable for

218 st vaccine strategy induced a Gag-specific T-cell response that was dominated by polyfunctional CD4(+

219 equences from one to three and related the T cell responses that recognize the immunodominant Tax pro

220 ndocardial cells to regulate the mesenchymal cell responses that remodel cardiac cushions to mature v

221 uced in the blood compared with intestine; T-cell responses that we detected had an increased frequen

222 ective vaccine elicited unconventional CD8 T cell responses that were entirely restricted by MHC II o

223 he mice to make adaptive CD4(+) and CD8(+) T cell responses that were necessary to clear the virus af

224 ute to radiation and cisplatin resistance of cells, responses that could be associated with cancer re

225 cells (DCs) are vital for the induction of T-cell responses, the DC subpopulations that induce Th2 ce

226 promote either tolerogenic or immunogenic T cell responses, the latter upon sensing microbes.

227 Although self-ligands directly affect GC B cell responses, the loss of Mer in dendritic cells promo

228 t studies have focused on the induction of T cell responses, the mechanisms by which targeting improv

229 Consistent with the magnitude of acute T-cell responses, the patient ultimately developed long-te

230 studies have characterized Ad5-induced CD8 T cell responses, there is a relative lack of detailed stu

231 We conclude that the T-cell response to brain metastases is not a surrogate of

232 -nitzschia multistriata, we investigated the cell response to cues released during sexual reproductio

233 d fibrinogen peptides, in the absence of a T cell response to fibrinogen.

234 DV serotypes (O, A, and Asia1 serotypes) a B cell response to FMDV SAT1 and serotype C was induced.

235 Thus, the potency of the T cell response to histoincompatible tissue is likely due

236 Understanding the stem cell response to immune therapies in ongoing human clini

237 The T-cell response to immunization was similar between genoty

238 ds in length can accurately identify a CD4 T cell response to ovalbumin against a background response

239 This study aimed to determine the T-cell response to Phl p 12 in profilin-sensitized patient

240 e cultured ELISPOT assay detected a higher T-cell response to pp65 than to IE-1 or IE-2, whereas in r

241 The HCMV-specific CD4(+) T cell response to pp65, IE1, IE2, and gB was predominantl

242 n humans is appropriate as a model for the T cell response to primary DENV2 infection.

243 y provides new tools for evaluating the host cell response to RV infections in real time and suggests

244 ccal enterotoxin B (SEB); ii) the human MAIT cell response to SEB is rapid and far greater in magnitu

245 we demonstrate single-cell analysis of tumor cell response to the chemotherapy drug doxorubicin.

246 +) cells, we observed a decrease in CD8(+) T cell response to the L. monocytogenes vaccine.

247 No effect on antibody or T-cell response to tissue antigens in the Ltab-Ncr3 could

248 targeting tumor stiffness or the endothelial cell response to tumor stiffening may help restore vesse

249 matically decreased the size of the CD8(+) T cell response to two immunodominant epitopes.

250 ade could be effective in modifying T- and B-cell responses to allografts.

251 Here, we describe B cell responses to C-PfCSP from European donors who under

252 s show that type I IFN can suppress CD8(+) T cell responses to cross-presented Ag by depleting cross-

253 tion in DCs is required to initiate CD8(+) T cell responses to dead cells and to induce effective ant

254 The functional heterogeneity of T cell responses to diverse antigens expressed at differen

255 taken into account when studying endothelial cell responses to flow in vivo.

256 response, underlining the heterogeneity of T cell responses to HDM allergens.

257 developed long-term, polyfunctional memory T-cell responses to Lassa virus.

258 kappaB pathway, resulting in poor in vitro T-cell responses to mitogens and antigens caused by reduce

259 and RP significantly increased the number of cell responses to NaCl, whereas no effect was observed w

260 Further studies will determine whether T cell responses to neoepitopes are major disease drivers

261 a of Crohn's disease patients can induce Th1 cell responses to promote colitis.

262 Moreover, IL-22 deficiency enhanced T cell responses to promote viral clearance, but increased

263 Our data demonstrate that T cell responses to rDENV2Delta30 are largely similar to t

264 way affects TG- and cornea-resident CD8(+) T cell responses to recurrent ocular herpesvirus infection

265 We found that myeloid cell responses to RPE injury occur in stages: (1) an ear

266 mune cell infiltration, the nature of immune cell responses to RPE injury remains undefined.

267 required for MAIT cell activation; iv) MAIT cell responses to SEB can occur in a T cell receptor (TC

268 HCV infection in hepatocytes exacerbates Tfr cell responses to subvert antiviral immunity.

269 r (TCR) locus that was required for CD8(+) T cell responses to the Plasmodium berghei GAP5040-48 epit

270 CD8(+) T cell responses to these genome-wide epitopes were compar

271 elp overcome immunosuppression and enhance T-cell responses to tumor antigens.

272 Here we examined CD4 T cell responses to two leading TB vaccine antigens, ESAT-

273 re proper programming of CD8(+) and CD4(+) T cell responses to viral infection.

274 T cell responses to viruses are initiated and maintained i

275 d MyD88 (CD8alpha:MyD88) to enhance CD8(+) T-cell responses to weakly immunogenic and poorly expresse

276 We show this strategy elicits potent T cell responses toward highly conserved internal Ags whil

277 rength, prevalence and cross-reactivity of T-cell responses towards Phl p 12 are comparable to the ma

278 portant role as APC-expanding autoreactive T cell responses ultimately causing type 1 diabetes (T1D).

279 Although IL-6 promoted virus-specific T cell responses, uncontrolled IL-6 expression in Ifitm3-/

280 mportant role in preventing inappropriate Th cell responses under normal conditions.

281 , which promote tissue eosinophilia and mast cell responses, undergo chemotaxis and cytokine producti

282 6 epitopes accounted for half of the total T cell response, underlining the heterogeneity of T cell r

283 of immunotherapies that boost pre-existing T cell responses, understanding how different immune cells

284 he kinetics of viremia resolution, the CD8 T-cell response was of surprisingly high magnitude and pro

285 increase in HDV-specific CD4(+) and CD8(+) T-cell responses was evident when the third signal cytokin

286 To assess whether CCR2 directly regulates T cell responses, we followed the fates of CCR2(-/-) T cel

287 /and IE(k)/SERCA2a 971-990 dextramers, the T cell responses were determined by flow cytometry to be A

288 feron-positive (IFN-gamma(+)) Gag-specific T-cell responses were dominated by CD4(+) T cells (P < 0.0

289 However, antibody and CD8(+) T cell responses were minimally affected.

290 lizing antibody (nAb) responses and CD8(+) T-cell responses were not significantly enhanced in the bn

291 HPV-16-specific CD8(+) T cell responses were significantly induced and negatively

292 Tumor-specific T cell responses were significantly lower in KT-CNI-SCC th

293 n had either a delayed or absent PD-1+ CD8 T-cell response, whereas 80% of patients with clinical ben

294 monomeric proteins elicit relatively poor B-cell responses which are short-lived.

295 n the antibody response than on the CD4(+) T cell response, which might influence the chosen strategy

296 (ROCK)2 downregulates the proinflammatory T cell response while increasing the regulatory arm of the

297 ditionally, both HCMV specific IgM and IgG B-cell responses with the ability to neutralize virus were

298 with clinical benefit exhibited PD-1+ CD8 T-cell responses within 4 wk of treatment initiation.

299 th induced and maintained antitumor CD8(+) T-cell responses within directly treated tumors and proved

300 displayed markedly reduced Ag-specific CD4 T cell responses within the local draining iliac lymph nod