ライフサイエンスコーパス: immune escape

1 nition and destruction by the immune system (immune escape).

2 virus's high sequence variability leading to immune escape.

3 n might represent a novel mechanism of tumor immune escape.

4 responded to the same CTL epitope and forced immune escape.

5 tructures while, at the same time, affording immune escape.

6 ression, proliferation, drug resistance, and immune escape.

7 amined the contribution of hypoxia to cancer immune escape.

8 gnaling in the regulation of hypoxia-induced immune escape.

9 lerizing signals evolve in cancer to promote immune escape.

10 t tissue damage but may also favor bacterial immune escape.

11 athogenic inflammatory processes that drives immune escape.

12 -A as an effective strategy to blunt tumoral immune escape.

13 adaptive immune responses and fosters tumor-immune escape.

14 ms for immunotherapeutic strategies to block immune escape.

15 cell epitopes, suggesting they promote viral immune escape.

16 ssed in malignant tumors and may favor tumor immune escape.

17 of strains with enhanced infectivity and/or immune escape.

18 tanding virus evolution, drug resistance and immune escape.

19 ysfunction plays an important role in cancer immune escape.

20 selection of antigenic variants in vivo, and immune escape.

21 istance to Fas-mediated apoptosis to promote immune escape.

22 tumor microenvironment acts as mechanism of immune escape.

23 osuppressive mechanisms that promote tumoral immune escape.

24 ses such as cancer that involve pathological immune escape.

25 es were readily neutralized, arguing against immune escape.

26 rtant role for CD4+ T-cell anergy in driving immune escape.

27 ly balancing replicative fitness and ongoing immune escape.

28 selected against in tumors as a mechanism of immune escape.

29 ed in the promotion of both tumor growth and immune escape.

30 sms in the tumor microenvironment that drive immune escape.

31 uits regulatory T (Treg) cells to facilitate immune escape.

32 cell death and promote T cell-mediated tumor immune escape.

33 tanding virus evolution, drug resistance and immune escape.

34 and processing of viral peptides, leading to immune escape.

35 ion, and lost antigen expression, indicating immune escape.

36 ew ranaviral genes involved in virulence and immune escape.

37 CTL recognition, illustrating a mechanism of immune escape.

38 ess linked to enhanced viral infectivity and immune escape.

39 lung epithelial cell apoptosis and promoting immune escape.

40 strategy that limits pathogen evolution and immune escape.

41 ion immunity, which in turn determines viral immune escape.

42 atitis B surface antigen (HBsAg), suggesting immune escape.

43 lationships between receptor specificity and immune escape.

44 t-network structure) is a key determinant of immune escape.

45 ay exist that reflect distinct categories of immune escape.

46 anti-tumor T cell response, contributing to immune escape.

47 to our understanding of the mechanism of HPV immune escape.

48 arget owing to its role in promoting tumoral immune escape.

49 a progression and chemoresistance, promoting immune escape.

50 ) response, which may contribute to H pylori immune escape.

51 stimulate T cell apoptosis as a mechanism of immune escape.

52 eir unique nature as exploited by tumors for immune escape.

53 recognize epitope variants and prevent viral immune escape.

54 ding motility, adhesion, transformation, and immune escape.

55 with those that support evolution of tumoral immune escape.

56 RCCs might exploit VCAM-1 overexpression for immune escape.

57 have also evolved strategies to thwart viral immune escape.

58 -proteins that might be exploited to prevent immune escape.

59 d mechanism that enables cancer stemness and immune escape.

60 n innate immune cell type also implicated in immune escape.

61 a new host through mutations that facilitate immune escape.

62 protein-1 (PD-1) leads to tumour-associated immune escape.

63 ir B-ALL, a novel mechanism of CD19-negative immune escape.

64 by herpes simplex virus 1 (HSV-1) for viral immune escape.

65 function as part of an acquired mechanism of immune escape.

66 y represent an additional strategy for viral immune escape.

67 les in viral replication, viral latency, and immune escape.

68 ants in the autologous virus consistent with immune escape.

69 t inefficient, mechanism of viral spread and immune escape.

70 that control inflammation and promote tumor-immune escape.

71 les in viral replication, viral latency, and immune escape.

72 l surface proteins, suggesting selection for immune escape.

73 nment (TME) is a major barrier to overcoming immune escape.

74 the concept of cancer immunosurveillance and immune escape.

75 hematopoietic cells by tumors contributes to immune escape.

76 ghts pertaining to risk and control of viral immune-escape: (1) replication rate and immune-stimulati

77 tigenic sin) act synergistically to increase immune escape, (2) immune-escape mutants with replicatio

78 ematically analyzed differential patterns of immune escape across all optimally defined epitopes in G

79 melanoma cells, where this event may enable immune escape after DNA damage.

80 reviously unexplored aspect of tumor-induced immune escape and a basis for biomarker development and

81 cytoid dendritic cells (pDC) that facilitate immune escape and correlate with poor prognosis.

82 o a new host species or to achieve antigenic immune escape and drug resistance.

83 ated upconversion nanoprobes (CC-UCNPs) with immune escape and homologous targeting capabilities are

84 phase variation could have a major impact on immune escape and host persistence of meningococci.

85 pread role of Ag processing mutations in HIV immune escape and identify molecular mechanisms underlyi

86 y independent genetic events, as a means for immune escape and immunotherapeutic resistance.

87 ns to understanding the relationship between immune escape and inflammation in cancer.

88 ed suppressor cells (MDSC), which facilitate immune escape and metastatic dissemination.

89 -attached regulators are relevant for innate immune escape and most likely contribute to tissue invas

90 ll nonresponsiveness is a critical factor in immune escape and myeloid-derived suppressor cells play

91 urrent treatments; and 2 genes, representing immune escape and proliferation, are the common features

92 e as a powerful clinical strategy to correct immune escape and promote therapeutic responses in breas

93 rategy to blunt Treg activity that can limit immune escape and promote tumor rejection.

94 ects of the contribution of hypoxia to tumor immune escape and provide evidence for a novel role of c

95 the decreased infectivity that may accompany immune escape and should be considered in studies assess

96 indings uncover a novel mechanism of tumoral immune escape and suggest that a soluble multivalent for

97 bit pleiotropic effects, orchestrating tumor immune escape and supporting RS cell survival.

98 oncogenic BRAF (BRAF(V600E)) contributes to immune escape and that blocking its activity via MAPK pa

99 , but its potential contributions to tumoral immune escape and therapeutic targeting have been less s

100 D73 expression in fibroblasts promotes tumor immune escape and thereby tumor growth.

101 ions between signaling pathways that control immune escape and those that control proliferation, sene

102 offer a novel generalized strategy to blunt immune escape and treat cancer.

103 Thus, our data demonstrate a novel immune escape and tumor growth-supporting mechanism medi

104 porting a link between ganglioside-dependent immune escape and tumor outgrowth.

105 ressive tumor microenvironment that promotes immune escape and tumor survival and growth.

106 ence on tumor growth by coordinately linking immune escape and tumorigenicity.

107 aques is associated with persistent viremia, immune escape, and AIDS.

108 oxia, enabling them to acquire mechanisms of immune escape, and as they move through the epithelial-m

109 luding motility, attachment, transformation, immune escape, and colony formation.

110 nificantly to HIV-1 evolution, pathogenesis, immune escape, and drug resistance.

111 ccumulate during tumor formation, facilitate immune escape, and enable tumor progression.

112 l subset of CCR2(+) Treg involved in tumoral immune escape, and they offer evidence that this Treg su

113 phan residues (e.g., Trp-57 and Trp-183) and immune escape-associated sites were responsible for redu

114 he model predicts an increase in the rate of immune escape at late stages of infection.

115 nding of factors driving viral evolution and immune escape at the population level.

116 been studied in relation to T cell-mediated immune escape, but their impact on NK cells via interact

117 opes, it is unknown whether selection-driven immune escape by CD4 T cell epitopes is a significant fa

118 activation of the AKT-mTOR pathway promotes immune escape by driving expression of PD-L1, which was

119 ing involvement of the PD-1/PD-L1 pathway in immune escape by hematopoietic cancers, such as acute my

120 ne of the important contributors to the host immune escape by HIV-1 through its ability to dysregulat

121 echanism for CD137L expression that mediates immune escape by HRS cells, and they identify CD137 as a

122 uveal melanoma, which may, in part, promote immune escape by impairing T-cell function.

123 has been shown to play a major role in tumor immune escape by inducing apoptosis of effector leukocyt

124 cells appears as a new possible mechanism of immune escape by lymphoma cells.

125 ng immune function that may be exploited for immune escape by pathogens and tumors.

126 Selective pressure against immune escape by pathogens can maintain appreciable freq

127 B7-H3 protein expression has implications in immune escape by solid tumors.

128 are important in promoting inflammation and immune escape by tumor cells.

129 ociated Ag (TAA) expression, associated with immune escape by tumors.

130 d that pathways of viral diversification and immune escape can be determined accurately.

131 would widen disease indications and prevent immune escape caused by the emergence of antigen-loss va

132 S-layer switching and immune escape could help explain temporal and geographic

133 Minimizing the degree of immune escape could represent a secondary benefit of eff

134 Immune escape describes a critical event whereby tumor c

135 Immune escape driven by selection pressure from virus-sp

136 utic vaccine strategies have been limited by immune escape due to HCV variants that are resistant to

137 We previously found that immune escape during acute SIV infection is conditional;

138 exclude a delayed immune response caused by immune escape established by HCMV strains.

139 host population level, despite the fact that immune-escape evolution involves dynamical processes tha

140 e now tested the hypothesis that conditional immune escape extends into chronic SIV infection and tha

141 ell-derived AML, including genes involved in immune escape, extravasation and small GTPase signal tra

142 been used to probe the mechanism underlying immune escape for influenza A virus-specific CD8(+) T ce

143 -ligand-1 (PD-L1), suggesting a mechanism of immune escape for TPCs.

144 ct as a preferred nodal modifier pathway for immune escape, for example analogous to the PI3K pathway

145 of aggressive antiretroviral treatment, HIV immune escape from CD8(+) T cell control can still devel

146 point to a role for hypoxia/HIF-1 in driving immune escape from CTL, and they suggest a novel cancer

147 show how miR-210 induction links hypoxia to immune escape from CTL-mediated lysis, by providing a me

148 nism by which hypoxia contributes to tumoral immune escape from cytotoxic T lymphocytes (CTL).

149 irect link between metastasis capability and immune escape from NK cells.

150 These observations describe a mechanism for immune escape from tumor dormancy in humans that relates

151 SIV and HIV share a fundamental mechanism of immune escape from vaccine-elicited or naturally elicite

152 This study reveals a novel immune-escape function for S. aureus-secreted proteins t

153 Continuous immune escape has been proposed as a mechanism of intrah

154 he HPV protein responsible for inducing this immune escape has not been determined.

155 its of B-cell depletion in combating tumoral immune escape have been debated.

156 tantly, our findings support the conditional immune escape hypothesis, such that the potential to pre

157 CR) among variants are inconsistent with the immune-escape hypothesis.

158 lymphocyte-deprived environment but promoted immune escape in a lymphocyte-enriched environment.

159 of S-3B drove tumorigenesis by facilitating immune escape in a manner associated with resistance to

160 hylogenetic trees with a weaker signature of immune escape in AIVs than in human viruses.

161 We propose TE suppression as a mechanism for immune escape in AML and MDS.

162 the transmembrane mucin MUC1 contributes to immune escape in an aggressive form of breast cancer, wi

163 e, we report mechanistic evidence of tumoral immune escape in an exemplary clinical case: a patient w

164 Briefly, we propose that genetic pathways of immune escape in cancer are synonymous with pathways tha

165 CD73 may promote immune escape in cancer by contributing to the degradati

166 rs on immune cells are pivotal regulators of immune escape in cancer.

167 opportunities for therapeutic corrections of immune escape in cancer.

168 hways controlled by this central mediator of immune escape in cancer.

169 ent, representing an additional mechanism of immune escape in cancer.

170 plicated in angiogenesis, proliferation, and immune escape in cancer.

171 , we show that CCL5 plays a critical role in immune escape in colorectal cancer.

172 cells, thereby defining a novel mechanism of immune escape in colorectal cancer.

173 ricted epitopes represents one mechanism for immune escape in HCV, many targeted epitopes remain inta

174 lts identify a novel role for PSC in driving immune escape in pancreatic cancer and extend the eviden

175 ritical to reverse an important mechanism of immune escape in patients with advanced melanoma.

176 ies to block cancer-related inflammation and immune escape in patients with RCC.

177 Overall, our study defines sites of immune escape in SIV in pigtailed macaques, and this ena

178 tope does not appear to affect the timing of immune escape in SIV.

179 ll epitopes within a single animal can delay immune escape in targeted epitopes.

180 r cell of a distant metastatic site requires immune escape in the new microenvironment.

181 Critical drivers of immune escape in the tumor microenvironment include tumo

182 Mechanisms of immune escape in this context are unknown.

183 K/E promoted drug resistance and facilitated immune escape in this setting.

184 r, our findings show how MUC1 contributes to immune escape in TNBC, and they offer a rationale to tar

185 results in a significant breakdown in tumor immune escape in various transplantation models and in a

186 our results illustrated a novel mechanism of immune escape in which tumor cells impede NK-mediated re

187 The epidemiological dynamics of immune-escape in acute-infection viruses with high trans

188 model is that HIV evolves a small number of immune escapes, in both relative and absolute terms, whe

189 mesenchymal transition, a known mechanism of immune-escape, in non-responding melanoma tumors.

190 e for the existence of an unrecognized tumor immune escape involving cross-presentation of systemical

191 n this study, we report a novel mechanism of immune escape involving tumor cell shedding of B7-H6, a

192 Immune escape is a critical gateway to malignancy.

193 Tumor immune escape is a critical trait of cancer but the mech

194 Immune escape is a fundamental trait of cancer in which

195 Immune escape is a fundamental trait of cancer.

196 Immune escape is a hallmark of cancer, but whether it re

197 Immune escape is an important reason why the immune syst

198 Immune escape is considered to be the driving force behi

199 ent knowledge of the types and mechanisms of immune escape is still incomplete.

200 Indeed, immune escape may be a central modifier of clinical outc

201 The data describe a novel immune escape mechanism and better define suitable targe

202 portantly, Treg cells served as the dominant immune escape mechanism early in tumor progression becau

203 ken together, our results illustrate a novel immune escape mechanism that can be activated by aberran

204 parallel events suggests that HLA LOH is an immune escape mechanism that is subject to strong microe

205 nce by the phagocytic cells, which may be an immune escape mechanism used by Plasmodium parasites tha

206 factor (HGF) can modulate the apoptosis and immune escape mechanism(s) of renal cancer cells by the

207 nterparts, indicating that the MYCN-mediated immune escape mechanism, which we believe to be novel, i

208 dent NK cell cytotoxicity as part of a tumor immune escape mechanism.

209 with vaccine-induced anti-HBs supporting an immune escape mechanism.

210 onounced upregulation of CD47 as a potential immune-escape mechanism and a significant downregulation

211 We now describe an immune-escape mechanism mediated by the inhibitory recep

212 le of ribose 2'-O-methylation as a potential immune-escape mechanism.

213 ent a homeostatic and compensatory "adaptive immune escape" mechanism acting as a nonneuronal determi

214 ent plays a central role in the evolution of immune escape mechanisms by tumor cells.

215 antimicrobial use, where drug resistance and immune escape mechanisms coevolve, thus increasing the l

216 ypic features have been linked to tumor cell immune escape mechanisms in PMBCL.

217 binatorial attack on advanced cancers, where immune escape mechanisms likely provide pivotal support.

218 cancer patients, and are limited by numerous immune escape mechanisms of tumor cells selected during

219 Thus, identifying the immune escape mechanisms responsible for inducing tumor-

220 However, the immune escape mechanisms used by malignant brain tumors

221 nity by TA-targeted mAb, in conjunction with immune escape mechanisms used by tumor cells, may contri

222 ls indicates that they have developed potent immune escape mechanisms.

223 r/virus-infected cells, thus contributing to immune escape mechanisms.

224 d the molecular basis of these 2 epitopes in immune-escape mechanisms and host-virus interactions are

225 t an important cellular mechanism of tumoral immune escape mediated by MDSCs and TAM in cancer.

226 netic study revealed a critical role for the immune escape mediator indoleamine 2,3-dioxygenase (IDO)

227 ulating anti-tumor immune suppression, tumor immune escape, metastasis and relapse, are considered an

228 Hepatitis B virus immune escape mutants have been associated with vaccine

229 ent of antiviral-resistant variants and host immune escape mutants.

230 The immune-escape mutants emerge frequently, displacing or c

231 nergistically to increase immune escape, (2) immune-escape mutants with replication deficiencies rela

232 ome the secretion defect caused by the G145R immune-escape mutation or mutation at N146, the site of

233 A viral population with >/=1 immune-escape mutation was found in 53.2% of patients (i

234 HBV genotype determination, and detection of immune escape mutations from a single contiguous HBV seq

235 entifying human immunodeficiency virus (HIV) immune escape mutations has implications for understandi

236 read of many-though not all-HIV-1 polymerase immune escape mutations in circulation over time.

237 fection, the virus typically evolves several immune escape mutations.

238 HBV genotype determination and detection of immune escape mutations.

239 CD8 T-cell epitopes that functionally act as immune escape mutations.

240 arent human leukocyte antigen (HLA)-mediated immune-escape mutations defined by older analysis method

241 ne pressure on viral diversity and potential immune-escape mutations.

242 ficulty is a considerable viral capacity for immune escape; new pandemic variants, as well as viral e

243 ys a role in tumor progression, with tumoral immune escape now well recognized as a crucial hallmark

244 irus (HBV) envelope gene are associated with immune escape, occult infection, and resistance to thera

245 Immune escape occurred with suboptimal vaccination, but

246 The timing of when immune escape occurs at a given epitope varies widely am

247 Despite very different patterns, immune escape occurs with a similar delay of on average

248 HAART was associated with increased risk of immune escape of 1.9-fold per log(10) viral load increme

249 Applied to the immune escape of a simian immunodeficiency virus epitope

250 and CD200 receptor, have been implicated in immune escape of cancer cells.

251 ex in gastric macrophages contributes to the immune escape of H. pylori.

252 The evolutionary speed and the consequent immune escape of H3N2 influenza A virus make it an inter

253 of the JCI, Bailey and colleagues show that immune escape of HCV can occur by naturally occurring po

254 tocompatibility complex-1 downregulation and immune escape of HIV-infected cells required for functio

255 ays a specific role in the induction of this immune escape of HPV16 through the manipulation of LC.

256 s few therapeutic options, and mechanisms of immune escape of recurring leukemic cells remain poorly

257 anistic insights, to our knowledge, into the immune escape of the influenza virus.

258 oleamine 2,3-dioxygenase 1 (IDO1), promoting immune escape of tumors, is a therapeutic target for the

259 show that viral lineage effects rather than immune escape often explain apparent human leukocyte ant

260 A key reason is the virus capacity for immune escape: ongoing evolution allows the continual ci

261 owing evidence suggests that, while numerous immune escape pathways are shared between hematological

262 Our work defines the immune escape pathways in which simultaneous blockade co

263 nts as a strategy to overcome locally active immune escape pathways.

264 The finding of upregulated immune-escape pathways, which may be responsible for sur

265 iral dynamic exists between the advantage of immune escape, peptide cross-reactivity, and the disadva

266 with PIDs do not reflect an increased tumor immune escape per se.

267 ons that together altered cell infection and immune escape properties of the viruses.

268 odel, most escapes also occur early, and the immune escape rate becomes small later, and typically on

269 analysis and mathematical modeling of virus immune escape showed that the contribution of CD8 T cell

270 e escapes evolve early, and that the rate of immune escape slows down considerably.

271 To investigate why the evolution of immune escape slows down over the time of infection, we

272 Tryptophan degradation is an immune escape strategy shared by many tumors.

273 The immune-escape strategy employed by human oncogenic adeno

274 Given the clinical correlates of immune escape, such heterogeneity suggests that certain

275 could be exploited for immunotherapy against immune-escaped, TAP-deficient tumor cells expressing low

276 etting in which to investigate mechanisms of immune escape that allow for viral persistence.

277 ition of NKT cells represents a mechanism of immune escape that can be reversed by adoptive immunothe

278 Our results reveal a novel mechanism of immune escape that supports tumor growth, with broad imp

279 le progress in elucidating its role in tumor-immune escape, the mechanisms underlying the inhibitory

280 T cell population, influences the timing of immune escape, thereby providing the first example of co

281 e germinal center reaction (TNFRSF14, IRF8), immune escape (TNFRSF14), and anti-apoptosis (MAP2K1) ha

282 ogenes directly orchestrate inflammation and immune escape to drive the multistep process of cancer p

283 resistance, DNA damage response, metastasis, immune escape, tumor angiogenesis, the Warburg effect an

284 Many oncogenes promote immune escape, undermining the effectiveness of immunoth

285 cells, we hypothesized that one mechanism of immune escape used by tumors involves the synthesis and

286 Here, we identify a new mechanism of tumor immune escape using an in vivo selection strategy.

287 ding viral pathogenesis and the emergence of immune escape variants and for design of vaccine strateg

288 Patterns of immune escape variants are similar in HIV type 1-infecte

289 tions, which give rise to drug-resistant and immune escape variants.

290 ss is a key contributor for the selection of immune escape variants.

291 in prevalence of subtypes/genotypes and drug/immune-escape variants were characterized by comparing r

292 via convergent microevolution, appear to be immune-escape variants, and were evolutionarily constrai

293 in lung cancer progression, acting to drive immune escape via a C3/C5-dependent pathway.Significance

294 mportant for successful infection, including immune escape via down-regulation of class I major histo

295 This example is the first on viral immune escape via exploitation of a "hole" in the T cell

296 or transcriptional co-repressors, along with immune escape via T-cell-mediated tumor surveillance.

297 Study topics include drug resistance, immune escape, viral emergence, host jumps, mutation eff

298 When we analyzed the kinetics of immune escape, we found that multiple escape mutants eme

299 t alter the tumor microenvironment to enable immune escape, we used small interfering RNA and small-m

300 involving the HLA locus suggestive of clonal immune escape were found in 3 of 93 patients with AA.