ライフサイエンスコーパス: immune control

1 lands independent of antiviral NK and T cell immune control.

2 bout the mechanisms used by tumors to escape immune control.

3 l interactions and does not require adaptive immune control.

4 opic lymphoid structures was associated with immune control.

5 t causal variants associated with favourable immune control.

6 n of Env responses associated with effective immune control.

7 TING-mediated cell death in T cells to evade immune control.

8 ssive replication, may be more vulnerable to immune control.

9 nterfering with dendritic cell (DC)-mediated immune control.

10 ll response breadth alone cannot account for immune control.

11 oll on virus replication are instrumental in immune control.

12 loss of CD4(+) and CD8(+) T cells abolished immune control.

13 specificity with environmentally responsive immune control.

14 ART interruption was then analyzed to assess immune control.

15 h levels of CXCL12 allows the tumor to evade immune control.

16 strategy employed by viruses to escape host immune control.

17 an important mechanism of tumor escape from immune control.

18 escape can play a causal role in the loss of immune control.

19 ral immune responses that may be involved in immune control.

20 iral escape mutants, with consequent loss of immune control.

21 cape from CTL recognition can undermine this immune control.

22 ymphocyte receptor expression to disarm host immune control.

23 n DCs to disturb their homeostasis and evade immune control.

24 lade-B virus was coincident with the loss of immune control.

25 erimental model for dissecting mechanisms of immune control.

26 of CD4+ but not CD8+ T cells also abrogated immune control.

27 ceptible form, suggesting inadequate in vivo immune control.

28 ree survival that is suggestive of long-term immune control.

29 the presence of epitopes relevant to natural immune control.

30 ory T cells (Tregs) are crucial mediators of immune control.

31 anti-HBs, anti-HBc), consistent with partial immune control.

32 ytes (CTLs) is a major barrier for effective immune control.

33 apillomavirus disease, progression, and host immune control.

34 he viral inoculum resulted in more efficient immune control.

35 cytes (CTLs) is a major barrier to effective immune control.

36 human viral infection, and may contribute to immune control.

37 fering with the dendritic cell (DC)-mediated immune control.

38 ch ensures efficient viral avoidance of host immune controls.

39 viral vulnerability might facilitate better immune control after preventive and therapeutic vaccinat

40 epresent both a major reason for loss of HIV immune control and a considerable challenge for HIV-1 va

41 ach thereby provides a mechanistic basis for immune control and a means to identify CD8(+) T cell epi

42 ed significant T cell-mediated, EBV-specific immune control and Ab production.

43 How loss of local immune control and bacterial dissemination is sensed and

44 responses have been shown to play a role in immune control and clearance of West Nile virus (WNV) in

45 strategies to detect, modulate, and/or evade immune control and clearance.

46 a potentially powerful strategy to establish immune control and eradicate persistent viral infections

47 host genetic contribution to the pattern of immune control and escape during HIV-1 infection.

48 become edited when they spontaneously escape immune control and grow into clinically apparent tumours

49 round against which other viruses can escape immune control and induce tumors.

50 rating stromal components interfere with the immune control and instruct immune cells to support, rat

51 an important model to dissect mechanisms of immune control and investigate vaccine strategies.

52 in potent CD4+ and CD8+ T cell-mediated EBV immune control and may be a promising clinical approach.

53 RIM58 as a novel negative mediator of innate immune control and mucosal homeostasis via TLR2 signalin

54 virus-infected subjects with HLA-B*57:01 to immune control and observed that a detectable KF11 respo

55 al cancer cells, renders them susceptible to immune control and provokes a shift in the tumor inflamm

56 of multiple tissues, impacting both ongoing immune control and restorative immune therapies.

57 ciently facilitates the escape of virus from immune control and the collapse of the whole immune syst

58 The balance between host immune control and viral immune evasion is pivotal to vi

59 relationship between HLA, T-cell activation, immune control, and HIV pathogenesis.

60 mechanistic analysis of virus pathogenesis, immune control, and prophylactic vaccine development.

61 However, mechanisms of immune control are poorly understood.

62 or neoantigens (TNAs) should be under robust immune control as they surge.

63 facilitate the elucidation of mechanisms of immune control, as well as accelerate the iterative test

64 cells provide both immediate tissue-specific immune control at the pathogen entry site and a more fle

65 CD8(+) T cells require 2B4 for EBV-specific immune control, because 2B4 blockade after CD8(+) T-cell

66 t lead to therapy resistance and escape from immune control before establishing acquired resistance g

67 The improved immune control by activated NK cells prolonged survival

68 n of adjuvant signals that ultimately elicit immune control by CD8(+) T lymphocytes.

69 However, tumors often evade immune control by crippling normal DC function.

70 of Nef during acute infection contributes to immune control by disrupting the function of Nef.

71 d it constitutes another layer of fine-tuned immune control by HIF that can dictate myeloid cell and

72 recognition, which enables virus escape from immune control by mutation in infections such as the hum

73 Hit and stay viruses evade immune control by sequestration, blockade of antigen pre

74 he rate of epithelial cell movement is under immune control by the cytokine interleukin-13 and the ch

75 se data demonstrate that p50 is required for immune control by the host and has distinct tissue-depen

76 Immune control can be facilitated by induction of autoph

77 bility of the target-cell population and the immune control characteristic of long-term non-progressi

78 Loss of this immune control coincides with a final escalation of the

79 Although long-term immune control could not be examined in this SHIV infect

80 s SIV-specific CD8(+) T cells for evaluating immune control during acute infection and demonstrate th

81 ions suggests the evasion of MyD88-dependent immune control during cervical carcinogenesis.

82 However, the correlates of immune control during chronic CMV infection remain incom

83 acity of high-risk LTRs to establish durable immune control during early chronic infection and provid

84 the capacity of high-risk LTRs to establish immune control during early chronic infection.

85 IGH) Tfh cells in lymph nodes correlate with immune control during infection, and their loss or dysre

86 represents a powerful approach to establish immune control during persistent infection, it is import

87 to antigen, which contributes to accelerated immune control during secondary infections.

88 es for the restoration of altered balance of immune control during T1D.

89 Despite increasing evidence that antitumor immune control exists in the pediatric brain, these find

90 ONCLUSIONThese observations demonstrate that immune control following ACT requires significant repert

91 virus but clearly distinguish patients with immune control from those without such control is of par

92 f these responses, but whether this enhances immune control has not been determined.

93 ever, the mechanisms of HLA-B*52:01-mediated immune control have not been well studied.

94 term positive trend in the intensity for the immune-controlled helminth, as immunity reduces the net

95 tion of Gag-specific CTL responses to better immune control if a sufficient multiplicity of infection

96 ty, with a focus on understanding how innate immune control impacts infection outcome and disease.

97 ucosa might partially explain the failure of immune control in AIDS.

98 the primary mechanism of virus evasion from immune control in B(*)5701(+) HIV-infected patients.

99 es could contribute to compromise antifungal immune control in chronic granulomatous disease patients

100 mmunotherapy holds promise for strengthening immune control in CML but requires the identification of

101 ontrols the balance of viral replication and immune control in favor of CD8 T-cell-mediated protectiv

102 tified as a crucial part of the EBV-specific immune control in healthy individuals.

103 The strongest genetic influence on immune control in HIV-1 infection is the HLA class I gen

104 Few studies have addressed the mechanisms of immune control in HIV-infected subjects in India, where

105 ion and underscore the strength and depth of immune control in limiting LCV-induced lymphoproliferati

106 (NK) cells are implicated as determinants of immune control in many viral infections, but the precise

107 The apparent loss of initial T cell-mediated immune control in the absence of B cells was investigate

108 role for CCR3-dependent eosinophil influx in immune control in the absence of IL-4/IL-13-dependent im

109 required for the initiation of EBV-specific immune control in vivo and that future EBV vaccine strat

110 exposed to a plethora of triggers requiring immune control, including a diverse commensal microbiome

111 multiple alterations associated with better immune control: increased infiltration and activation of

112 Rather, immune control is associated with the efficient establis

113 duced transition from immunotolerance to HBV immune control is characterized by the emergence of effi

114 Pulmonary immune control is crucial for protection against pathoge

115 The disease associated with loss of immune control is distinct from that seen during the acu

116 conserved HIV sequence, its association with immune control is not as strong.

117 Understanding the mechanisms underlying this immune control is of critical importance, yet they remai

118 ine-induced cellular immunity and in natural immune control is of relevance for vaccine design.

119 II-restricted CD4(+) T cell responses to HIV immune control is poorly defined.

120 While their importance for proper immune control is undeniable, the stability of the Treg

121 e associated with lowering viremia; however, immune control is undermined by viral escape mutations.

122 al, including enhancement of vector-mediated immune control, manipulation of the insect microbiome, o

123 of cancer, and that mechanisms of overcoming immune control may be quite different from those at the

124 ecting strain of HIV to overcome preexisting immune control may be related to its ability to rapidly

125 uggest that a single definitive correlate of immune control may not exist; rather, a successful CD8(+

126 ives of their hosts in the face of effective immune control measures for productively infected cells.

127 sexually and cause congenital birth defects, immune control mechanisms in the female reproductive tra

128 viruses have learned how to manipulate host immune control mechanisms.

129 ts of CMV, this does not necessarily lead to immune control mediated via recognition of this genetic

130 Innate immune control, mediated in part by alpha-defensins expr

131 mmune response through a mesenchyme-mediated immune control (MMIC) mechanism.

132 t control MHCII expression and promote tumor immune control; mutational inactivation of CREBBP, but n

133 y understood mechanisms including incomplete immune control mutations of the HBsAg antigenic determin

134 the vital contributions of NK cells to HIV-1 immune control, nongenetic NK cell parameters directly a

135 (DCs), critical antigen-presenting cells for immune control, normally derive from bone marrow precurs

136 atients off-therapy, suggesting the restored immune control observed in MMR and MR(4.5) is not an ent

137 ion but allows for improved NK cell-mediated immune control of a human gamma-herpesvirus.

138 These data demonstrate that durable partial immune control of a pathogenic SIV challenge for more th

139 versity in T/F genomes could regulate innate immune control of acute HCV infection.

140 T cell responses are crucial for subsequent immune control of acute infection, which has important i

141 ences between immunity to virus exposure and immune control of an established viral infection and fur

142 ncy virus (SIV) Gag afforded durable partial immune control of an SIV challenge in rhesus monkeys.

143 of BKPyV, questioning a role for MICA in the immune control of BKPyV infection.

144 he tumor inflammatory milieu associated with immune control of cancer and establish a strategy to pre

145 ates with checkpoint blockade and allows for immune control of cancers with low nonsynonymous mutatio

146 rse signaling in NK cells contributes to the immune control of CD27-expressing B-cell lymphoma and le

147 eritance of genes that are beneficial in the immune control of cerebral malaria but that, in the abse

148 t connection between DNA damage response and immune control of chronic gammaherpesvirus infection, a

149 CD8(+) T cells is a significant obstacle to immune control of chronic infections or tumors.

150 Our results suggest that protective immune control of chronic infections, like EBV, includes

151 y, these results suggest that more effective immune control of chronic type II infection in the genet

152 rimary infection are important predictors of immune control of CMV during early chronic infection.

153 ur data provide a clear demonstration of the immune control of CMV in immunosuppressed patients and e

154 ecific T-cell immunity in healthy donors and immune control of disease.

155 mechanisms underlying viral replication and immune control of diverse HIV-1 strains.

156 ction play a similar significant role in the immune control of dual HIV-1 and HIV-2 infection.

157 Therefore immune control of each cycle would require responses to

158 reconstituted mice improved NK cell-mediated immune control of EBV infection, indicating that mixed h

159 and persistent EBV infection, their role in immune control of EBV replication is not known.

160 suggests that these CTL may be important for immune control of EBV-related gamma-herpesvirus infectio

161 Instead, immune control of EIAV infection during the clinically i

162 a finding indicative of tight but incomplete immune control of EIAV replication.

163 lls will aid in dissecting mechanisms of CD4 immune control of gamma-herpesvirus latency and the deve

164 CD4 T cells are essential for immune control of gamma-herpesvirus latency.

165 This could reduce immune control of HBV and lead to chronic infection.

166 erentially expanded in patients with partial immune control of HBV infection and can remain in the li

167 regions by HLA-B27 in its ability to assert immune control of HCV and other highly variable pathogen

168 f4 in CD11c(+) DCs results in more efficient immune control of Helicobacter pylori, Mycobacterium bov

169 The immune control of hepatitis B virus (HBV) infection is e

170 Leukocytes participate in the immune control of herpes simplex virus (HSV).

171 HLA-B*57 is strongly associated with immune control of HIV and delayed AIDS progression.

172 Immune control of HIV at an individual level is strongly

173 izing and non-neutralizing antibodies in the immune control of HIV infection as well as for the devel

174 s about which immune responses contribute to immune control of HIV infection.

175 may be of overriding importance in achieving immune control of HIV infection.

176 er the role of reverting escape mutations in immune control of HIV infection.

177 eg-cell number and/or function could improve immune control of HIV infection.

178 Cellular immune control of HIV is mediated, in part, by induction

179 hat HLA-B molecules that are associated with immune control of HIV principally target conserved epito

180 hrough epitope mutations can lead to loss of immune control of HIV replication.

181 function co-operatively to result in greater immune control of HIV than mediated by either single all

182 with HLA class I alleles mediating effective immune control of HIV through the number of p24 Gag-spec

183 r T lymphocytes (HTL) play a key role in the immune control of HIV type 1 (HIV-1) infection, and as s

184 rapy, efforts to eradicate viral reservoirs, immune control of HIV, and Ag-specific immune defects.

185 tter define the mechanisms of the HLA-B 2705 immune control of HIV, we first characterized the CD8(+)

186 served differences in HLA-B*57/5801-mediated immune control of HIV, we undertook, in a study of >1,00

187 Differences in immune control of HIV-1 infection are often attributable

188 CD4 T-cell responses contribute to effective immune control of HIV-1 infection.

189 tionalize how TRIM5alpha participates in the immune control of HIV-1 infection.

190 ne correlate-thus implicating polyfunctional immune control of HIV-1 transmission.

191 le and thus may be important targets for the immune control of HIV-1-infection and for effective vacc

192 more effective vaccines capable of inducing immune control of HIV-1.

193 novel component of sex differences in innate immune control of HIV-1.

194 topes that may play an important role in the immune control of HIV-1.

195 opolymorphisms, have a significant impact on immune control of HIV.

196 responses, are also critically important to immune control of HIV.IMPORTANCE In HIV infection, altho

197 meterize and test mathematical models of the immune control of HTLV-1, which are a necessary part of

198 The stable immune control of human immunodeficiency virus (HIV) in

199 polymorphism that has the greatest impact on immune control of human immunodeficiency virus (HIV) inf

200 cytotoxic T lymphocytes (CTLs) can undermine immune control of human immunodeficiency virus 1.

201 The association between HLA-B 2705 and the immune control of human immunodeficiency virus type 1 (H

202 Immune control of human immunodeficiency virus type 1 (H

203 experimental model system to study the host immune control of infection and explore novel vaccine st

204 nterruptions has shown promise for enhancing immune control of infection.

205 immune system, thereby preventing effective immune control of infection.

206 on of escape mutations has a major impact on immune control of infections with viruses such as human

207 -Th2 polarization differentially affects the immune control of intracellular pathogens.

208 le during acute infection, are essential for immune control of latency and persistent replication.

209 and humoral CMV-specific immune responses in immune control of latent CMV infection was evaluated pro

210 nant T cell response plays a key role in the immune control of latent virus.

211 or the effect of tolerance protocols on the immune control of latent viruses.

212 CD4 T cells are required for complete immune control of long-term infection, in part by provid

213 Th cells most likely contributes to loss of immune control of LTBI in HIV-infected individuals, alth

214 ll non-Hodgkin lymphoma, but its role in the immune control of lymphoma and leukemia is unknown.

215 Insight into the immune control of M. abscessus may provide novel targets

216 icate that SP-A and SP-D are dispensable for immune control of M. tuberculosis in a low-dose, aerosol

217 gly identified no gross defects in uptake or immune control of M. tuberculosis in SP-A-, SP-D-, and S

218 l function and the impact of this biology on immune control of malignancies.

219 Immune control of many intracellular pathogens, includin

220 s, which in turn contribute to the effective immune control of many viral infections.

221 d the length of the equilibrium phase during immune control of methylcholanthrene (MCA)-induced or p5

222 al therapy (cART) reduces LTBI reactivation, immune control of Mtb is not fully restored, as shown by

223 D4 T cells are each critically important for immune control of murine gammaherpesvirus 68 (gammaHV68)

224 Immune control of Mycobacterium tuberculosis depends on

225 , and it provides insight into cell-mediated immune control of O. tsutsugamushi and dissemination dyn

226 cell deletion dynamics but may contribute to immune control of oncogenic gamma-herpesviruses.

227 at process could be a step toward preserving immune control of particularly persistent RNA viruses an

228 nal inflammation, autoimmunity, and impaired immune control of pathogenic bacteria and protozoa.

229 Immune control of PDA growth was achieved, however, by d

230 In healthy individuals, immune control of persistent human cytomegalovirus (HCMV

231 Immune control of persistent infection with Mycobacteriu

232 omical differences might account for lack of immune control of persistent pathogens, which suggests t

233 nderscore the importance of CD8+ CTLs in the immune control of persistent viral infections.

234 NK cells are critical for the innate immune control of poxviral infections.

235 a mouse CMV (MCMV) vector provides complete immune control of recombinant vaccinia virus expressing

236 e to detect both human herpesvirus (HHV) and immune control of replication post-solid organ transplan

237 tion, set point, and pathogenesis.IMPORTANCE Immune control of retroviruses is notoriously difficult,

238 CD8+ T cell responses are necessary for immune control of simian immunodeficiency virus (SIV).

239 viremia in naturally SIV-infected SMs, i.e., immune control of SIV replication versus target cell lim

240 ility of activated CD4+ T cells, rather than immune control of SIV replication, is the main determina

241 irming an important role for CCL5 in optimal immune control of T. cruzi replication at the point of i

242 ruzi, a property known to correlate with the immune control of T. cruzi.

243 Thus, TNF-dependent immune control of T. gondii expansion in the brain invol

244 response to Helicobacter pylori and impaired immune control of the bacteria.

245 NK cells play an important role in innate immune control of the infection with vaccinia virus (VV)

246 Therefore, tight immune control of the intraerythrocytic replication of t

247 mental model for understanding mechanisms of immune control of the latent human gammaherpesviruses.

248 Thus, immune control of the microbiota maintains beneficial mi

249 Immune control of the protozoan parasite Trypanosoma cru

250 ls and macrophages, might interfere with the immune control of the tumor.

251 s postinfection), suggestive of differential immune control of the two viruses.

252 important target for the host cell-mediated immune control of the virus during natural infection.

253 ory response in the airway without affecting immune control of the virus.

254 er, the molecular mechanisms responsible for immune control of their replication are not completely u

255 , has provided an in vivo model for studying immune control of these persistent viruses.

256 of central importance for characterizing the immune control of this infection.

257 t the role of primary EBV infection and poor immune control of this virus.

258 lta T cells because of the role they play in immune control of this virus.

259 hat are essential elements for detection and immune control of Toxoplasma gondii in mice, but not in

260 atopoietic and mesenchymal cells, suppresses immune control of tumor growth.

261 An emerging consensus is that immune control of tumors is mediated by cytotoxic CD8+ T

262 ce enhanced rather than inhibited the innate immune control of vaccinia virus (VV) replication.

263 Immune control of viral infections is heavily dependent

264 Immune control of viral infections is modulated by diver

265 ural killer cells are a key component in the immune control of viral infections.

266 totoxic T lymphocytes (CTLs) are crucial for immune control of viral infections.

267 ed HMPV titers in the lungs, suggesting some immune control of viral persistence.

268 ds to increased T cell function and improved immune control of viral replication.

269 e as a novel therapeutic approach to improve immune control of virus replication and mitigate age rel

270 nonprogressive disease, suggesting that the immune control of virus replication represents a balance

271 n vitro and that type I IFN-dependent innate immune control of VV infection in vivo was mediated by a

272 activation played a critical role in innate immune control of VV infection.

273 a critical role for type I IFN in the innate immune control of VV infection.

274 ncept that differential CD8+ T cell-mediated immune control of X4- and R5-SHIV replication is respons

275 compromises the in vivo cell death-dependent immune control of Yersinia infection, a physiological mo

276 By implementation of individual SS immune controls of non-permanent duration, the resulting

277 Loss of immune control opens the way to virus reactivation and d

278 CD8(+) T lymphocytes (CTLs) exert important immune control over HIV and so are a major selective for

279 ent with genetically engineered cells, exert immune control over HIV-1 replication, and identify and

280 tem which modeled the first steps of in vivo immune control over posttransplant lymphoproliferative d

281 etastases, while simultaneously jeopardizing immune control over residual malignant cells.

282 targeting of immunodominant Gag epitopes and immune control, particularly the contribution of a singl

283 c coronavirus due to loss of T cell-mediated immune control provided an experimental model to test T

284 population that persists during ART escapes immune control remains unknown.

285 60 smallpox-vaccinated (i.e., vaccinia virus-immune) control subjects.

286 HLA class I molecules mediating effective immune control, such as HLA-B*27 and HLA-B*57, are assoc

287 EBV infection and generates T cell-mediated immune control that resists oncogenic transformation.

288 se proteins are numerous factors involved in immune control, the complement cascade, and growth facto

289 es, but over time they evolve and can escape immune control through various mechanisms, including the

290 ng of the overall complexities of CD8 T-cell immune control throughout infection.

291 T cells are required for the development of immune control to T. cruzi, but that type 2 T cells cont

292 ch might render them uniquely susceptible to immune control upon neoplastic transformation, has not b

293 ypes resembling those associated with cancer immune control versus escape in mice.

294 ty and/or progression reflect an escape from immune control, very little is known about the phenotype

295 determined by the balance between antiviral immune control, viral replication, and immune-mediated d

296 No evidence of acquired resistance to immune control was found in 12 relapse reisolates.

297 influenza and human cytomegalovirus-specific immune control was unchanged in MS.

298 To facilitate the study of immune control, we sought an outbred and immunocompetent

299 After primary infection, 7 LTRs lacked immune control with relapsing viremia during early chron

300 To better understand the distinct phases of immune control within the CNS, the kinetics of humoral i