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 rs can only establish after the evolution of immune escape.

3 ysfunction plays an important role in cancer immune escape.

4 ess linked to enhanced viral infectivity and immune escape.

5 strategy that limits pathogen evolution and immune escape.

6 lationships between receptor specificity and immune escape.

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

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

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

10 have also evolved strategies to thwart viral immune escape.

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

12 d mechanism that enables cancer stemness and immune escape.

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

14 a new host through mutations that facilitate immune escape.

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

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

17 al platform in which to intervene to prevent immune escape.

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

19 y represent an additional strategy for viral immune escape.

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

21 ants in the autologous virus consistent with immune escape.

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

23 that control inflammation and promote tumor-immune escape.

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

25 l surface proteins, suggesting selection for immune escape.

26 the concept of cancer immunosurveillance and immune escape.

27 hematopoietic cells by tumors contributes to immune escape.

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

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

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

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

32 amined the contribution of hypoxia to cancer immune escape.

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

34 lerizing signals evolve in cancer to promote immune escape.

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

36 athogenic inflammatory processes that drives immune escape.

37 adaptive immune responses and fosters tumor-immune escape.

38 ms for immunotherapeutic strategies to block immune escape.

39 cell epitopes, suggesting they promote viral immune escape.

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

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

42 tanding virus evolution, drug resistance and immune escape.

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

44 d to enhancement of the viral life cycle and immune escape.

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

46 tumor microenvironment acts as mechanism of immune escape.

47 osuppressive mechanisms that promote tumoral immune escape.

48 ses such as cancer that involve pathological immune escape.

49 es were readily neutralized, arguing against immune escape.

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

51 ly balancing replicative fitness and ongoing immune escape.

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

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

54 sms in the tumor microenvironment that drive immune escape.

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

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

57 tanding virus evolution, drug resistance and immune escape.

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

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

60 that ultimately result in tumor clearance or immune escape.

61 for overcoming cancer therapy resistance and immune escape.

62 f significant antigenic variation leading to immune escape.

63 table to differential mutational barriers to immune escape.

64 nal landscape that promoted tumor growth and immune escape.

65 at niche breakdown may be a key mechanism of immune escape.

66 ariation is generated during persistence for immune escape.

67 of PD-1+/CD8+ T cell infiltrates, suggesting immune escape.

68 ce immunosuppressive metabolites, leading to immune escape.

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

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

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

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

73 ding of the evolution of cancer cells toward immune escape(1-5).

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

75 ls, which may shed light on the evolution of immune escape across tumor geographical locations, remai

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

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

78 indicate IFITM proteins as drivers of viral immune escape and antibody-mediated HCV neutralization i

79 HIV diversification facilitates immune escape and complicates antiretroviral therapy.

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

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

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

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

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

85 ate that PIMs support PMBL cell survival and immune escape and identify PIMs as promising therapeutic

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

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

88 ing, also have a key role in tumour-mediated immune escape and might, therefore, be potential targets

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

90 HCC will provide important insights into HCC immune escape and promote the development of biomarker-d

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

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

93 In summary, our data link the LSC concept to immune escape and provide a strong rationale for targeti

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

95 omprehensive dataset for understanding viral immune escape and refining therapies and vaccines.

96 nding of the molecular pathways connected to immune escape and relapse may help to improve our therap

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

98 ribute directly and indirectly to both tumor immune escape and the metastatic cascade.

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 s and will be instrumental to identify viral immune escape and to develop and monitor novel mitochond

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

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

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

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

106 further associate electrostatic charge with immune escape and viral evolutionary dynamics.

107 s variants can provide means for adaptation, immune escape and virus perpetuation.

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

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

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

111 Antigenic evolution facilitates H3N2 immune escape, and increasing glycosylation of the hemag

112 r Nef promotes high-titer viral replication, immune escape, and pathogenicity.

113 ells to eliminate the primary tumor, prevent immune escape, and provide long-term protective memory.

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

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

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

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

118 Immune escape by antigenic drift, in which viruses gener

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

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

121 ved suppressor cells (G-MDSCs) that mediated immune escape by impairing T cell response.

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

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

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

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

126 isplayed reduced clonality with emergence of immune escape clones.

127 rease our quantitative understanding of many immune escape contexts, including cancer progression and

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

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

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

131 This is counter-intuitive, since immune escape due to increased avidity (due itself to an

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

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

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

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

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

137 e TLR2-dependent endosomal signaling enabled immune escape for S. aureus, because this pathway, but n

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

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

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

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

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

143 uplicated pseudogene locus is sufficient for immune escape from the broad antibody response generated

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

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

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

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

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

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

150 -immunity and antigenic mutations that allow immune escape impact influenza epidemic dynamics at the

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

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

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

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

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

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

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

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

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

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

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

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

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

164 y the analysis of neoantigen frequencies and immune escape in exome and RNA sequencing data from 879

165 prevent tumor growth and TGFbeta1-dependent immune escape in high-risk neuroblastoma patients as wel

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

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

168 targeting in an effort to reduce the risk of immune escape in pediatric B-cell acute lymphoblastic le

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

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

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

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

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

174 Mechanisms of immune escape in this context are unknown.

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

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

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

178 ce some of the beneficial effects increasing immune escape in vivo.

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

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

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

182 elp identify immunogenic viral regions where immune escape incurs a fitness cost.

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

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

185 Immune escape is a fundamental trait of cancer in which

186 Immune escape is a fundamental trait of cancer.

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

188 n+venetoclax+anti-PD-1 treatment to overcome immune escape, led to durable antitumor responses even a

189 nserved NGS N262, N448, and N301, created an immune escape map of the conserved and variable sequons

190 expression on malignant cells is a dominant immune escape mechanism across a variety of human cancer

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

192 For MCC, one immune escape mechanism is insufficient for recognition

193 n in the tumor microenvironment generates an immune escape mechanism rendering NK cells inactive.

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

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

196 This argues for a novel humoral immune escape mechanism that may also have important imp

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

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

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

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

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

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

203 oenvironment and cancer cells contributes to immune escape mechanisms and drug resistance.

204 nto 4 TME-based subtypes related to distinct immune escape mechanisms and patient outcomes.

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

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

207 Mapping the immune escape mechanisms enacted by head and neck cancer

208 Targeting of tumor immune escape mechanisms holds enormous therapeutic pote

209 An in-depth understanding of immune escape mechanisms in cancer is likely to lead to

210 its growth, spreading, and TGFbeta-dependent immune escape mechanisms in neuroblastoma.

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

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

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

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

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

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

217 cells to kill cancer cells, however, several immune-escape mechanisms can be enacted by cancer cells

218 We divide the evidence in support of immune-escape mechanisms into animal studies, human labo

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

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

221 The in vitro immune escape mutant selection method used in this study

222 This study demonstrates that the immune escape mutants also (i) gained greater replicatio

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

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

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

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

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

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

229 As predicted, these immune escape mutations were also observed in the field

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

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

232 HBV genotype determination and detection of immune escape mutations.

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

234 scribe a widely underappreciated pathway for immune escape, namely immune-mediated dedifferentiation

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

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

237 Here we show that immune activation and immune escape occur before tumour invasion, and reveal t

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

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

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

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

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

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

244 Nef enhances viral replication and promotes immune escape of HIV-infected cells but lacks intrinsic

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

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

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

248 was assessed and their role in survival and immune escape of the tumor cells was determined.

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

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

251 N-I) induction has been proposed as one such immune escape pathway that may favor S. aureus Cell wall

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

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

254 jor B-cell lymphomas with an emphasis on the immune escape pathways orchestrated by these diseases.

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

256 signing vaccines which can effectively block immune escape pathways.

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

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

259 lular immunity, we hypothesized that certain immune-escape polymorphisms may impair Nef's ability to

260 odulate inflammatory responses, enable viral immune escape, promote cancer cell metastasis or regulat

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

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

263 owever, the clinical impact of IFITMs on HCV immune escape remains to be determined.

264 her tobacco carcinogens enable exposed cells immune escape resulting in carcinogenesis, and why patie

265 ctivation of VEGFR3 signaling fosters cancer immune escape, resulting in enhanced tumor growth.

266 f immune pressure on the clonal dynamics and immune escape signature by comparing glioma growth in im

267 The identified murine immune escape signature was reflected in human patients

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

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

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

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

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

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

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

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

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

277 ; (3) the activation of immune responses and immune escape through immune checkpoints and suppressive

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

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

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

281 The model predicts that, without immune escape, tumor neoantigens are either clonal or at

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

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

284 n Env from HIV-transmitted/founder (T/F) and immune escape variants and their mutants involving the N

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

286 ts) in NGS heterogeneity between the T/F and immune escape variants defined a range of NGS that we fu

287 ains residues frequently mutated in clinical immune escape variants, provides a molecular explanation

288 binations that may allow the anticipation of immune escape variants.IMPORTANCE The Env protein of HIV

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

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

291 study can facilitate the generation of host immune escape vectors.

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

293 d that CD40L(+) CAR T cells circumvent tumor immune escape via antigen loss through CD40/CD40L-mediat

294 hanism contributing to immunosuppression and immune escape via interacting with program death-1 (PD-1

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

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

297 The analysis showed that the emergent immune escape viruses contained mutations A125T, A151T,

298 e of homologous ferret antiserum resulted in immune escape viruses containing amino acid substitution

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

300 ese mechanisms, and therapeutic targeting of immune escape, will be discussed.