ライフサイエンスコーパス: immune control

1 n of Env responses associated with effective immune control.

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

3 apillomavirus disease, progression, and host immune control.

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

5 ll response breadth alone cannot account for immune control.

6 oll on virus replication are instrumental in immune control.

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

8 he viral inoculum resulted in more efficient immune control.

9 specificity with environmentally responsive immune control.

10 ART interruption was then analyzed to assess immune control.

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

12 strategy employed by viruses to escape host immune control.

13 an important mechanism of tumor escape from immune control.

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

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

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

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

18 cape from CTL recognition can undermine this immune control.

19 ymphocyte receptor expression to disarm host immune control.

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

21 erimental model for dissecting mechanisms of immune control.

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

23 ceptible form, suggesting inadequate in vivo immune control.

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

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

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

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

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

29 l interactions and does not require adaptive immune control.

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

31 opic lymphoid structures was associated with immune control.

32 t causal variants associated with favourable immune control.

33 ch ensures efficient viral avoidance of host immune controls.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 The improved immune control by activated NK cells prolonged survival

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

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

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

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

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

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

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

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

61 Immune control can be facilitated by induction of autoph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

91 Rather, immune control is associated with the efficient establis

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 Therefore immune control of each cycle would require responses to

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

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

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

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

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

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

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

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

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

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

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

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

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

145 Immune control of HIV at an individual level is strongly

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Immune control of human immunodeficiency virus type 1 (H

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 Immune control of many intracellular pathogens, includin

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

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

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

191 Immune control of Mycobacterium tuberculosis depends on

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

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

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

195 Immune control of persistent infection with Mycobacteriu

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

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

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

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

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

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

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

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

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

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

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

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

208 Immune control of the protozoan parasite Trypanosoma cru

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

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

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

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

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

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

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

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

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

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

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

220 Immune control of viral infections is heavily dependent

221 Immune control of viral infections is modulated by diver

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 60 smallpox-vaccinated (i.e., vaccinia virus-immune) control subjects.

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

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

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

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

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

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

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

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

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

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

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

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

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