ライフサイエンスコーパス: tuberculosis infection

1 sistent state of this pathogen during latent tuberculosis infection.

2 sis prevalence or who had evidence of latent tuberculosis infection.

3 set that may contribute to the control of M. tuberculosis infection.

4 rotection in a murine model of Mycobacterium tuberculosis infection.

5 robust T cell response observed during an M. tuberculosis infection.

6 ated with increased susceptibility to latent tuberculosis infection.

7 ving type I IFN responses and controlling M. tuberculosis infection.

8 ve autophagy of Mtb and host defense against tuberculosis infection.

9 variability in the response to Mycobacterium tuberculosis infection.

10 g is essential for the optimal control of M. tuberculosis infection.

11 been poorly characterized in the context M. tuberculosis infection.

12 nd demonstrated efficacy in a mouse model of tuberculosis infection.

13 terial growth during the chronic phase of M. tuberculosis infection.

14 layer in establishing this balance during M. tuberculosis infection.

15 omparable to those seen in cases of human M. tuberculosis infection.

16 increase in the risk of multidrug-resistant tuberculosis infection.

17 alize IL-10 in cynomolgus macaques during M. tuberculosis infection.

18 -cell responses and susceptibility to latent tuberculosis infection.

19 ritical for IFN-gamma-mediated control of M. tuberculosis infection.

20 8 years) recommended for treatment of latent tuberculosis infection.

21 e 2 vaccines yielded stronger immunity to M. tuberculosis infection.

22 rom 22 individuals with latent Mycobacterium tuberculosis infection.

23 e complication associated with Mycobacterium tuberculosis infection.

24 s of two macrophage models in response to M. tuberculosis infection.

25 tion time points during the first 6 mo of M. tuberculosis infection.

26 among individuals with latent Mycobacterium tuberculosis infection.

27 g 6859 adult participants with Mycobacterium tuberculosis infection.

28 ates CD8(+) T-cell function during latent M. tuberculosis infection.

29 entine for treatment of latent Mycobacterium tuberculosis infection.

30 f 1,25(OH)2D3 would affect the outcome of M. tuberculosis infection.

31 r important insights into early events of M. tuberculosis infection.

32 t is widely used as a test for Mycobacterium tuberculosis infection.

33 are bactericidal in a mouse model of chronic tuberculosis infection.

34 d fewer Ag-producing bacteria than during M. tuberculosis infection.

35 ed in subjects with HIV-associated active M. tuberculosis infection.

36 ntrols), pulmonary tuberculosis (PTB) and M. tuberculosis infection.

37 ssion of tuberculosis among patients with M. tuberculosis infection.

38 nize and inhibit intracellular Mycobacterium tuberculosis infection.

39 utilize aerobic glycolysis in response to M. tuberculosis infection.

40 hanisms and enhances host defense against M. tuberculosis infection.

41 lung granulomas of animals exhibiting latent tuberculosis infection.

42 s) who were eligible for treatment of latent tuberculosis infection.

43 ty does not correlate with the outcome of M. tuberculosis infection.

44 NE as a therapeutic approach early during M. tuberculosis infection.

45 bacterial burden and disease pathology in M. tuberculosis infection.

46 y a critical role in host defense against M. tuberculosis infection.

47 entral role in determining the outcome of M. tuberculosis infection.

48 trolled (latent) versus uncontrolled (TB) M. tuberculosis infection.

49 .15]) among those with a positive result for tuberculosis infection.

50 about the physiology of latent Mycobacterium tuberculosis infection.

51 in-derived host metabolic-fitness towards M. tuberculosis infection.

52 in the lung is not sufficient to control M. tuberculosis infection.

53 the management of latent multidrug-resistant tuberculosis infection.

54 ogic features suggestive of past evidence of tuberculosis infection.

55 ribute to the pathogenesis of progressive M. tuberculosis infection.

56 o effective in vivo with mouse models of MDR tuberculosis infection.

57 ible and drug-resistant latent and active M. tuberculosis infection.

58 a drug target to assist in the clearance of tuberculosis infection.

59 is is a clinically important complication of tuberculosis infection.

60 challenge for the treatment of Mycobacterium tuberculosis infections.

61 combination with rifapentine to treat latent tuberculosis infections.

62 CI, 1.09-4.89) were associated with mixed M. tuberculosis infections.

63 I, 2.48-41.71) were associated with mixed M. tuberculosis infections.

64 and the ability to control infection (latent tuberculosis infection, 62%; posttuberculosis patients,

65 of patients with asymptomatic Mycobacterium tuberculosis infection, a novel 3-gene transcriptional s

66 ically validated target for the treatment of tuberculosis infections, a disease that still causes the

67 ned children who had negative results for M. tuberculosis infection according to the QuantiFERON-TB G

68 e multiple immune sources of IL-10 during M. tuberculosis infection, activated effector T cells are t

69 lates the macrophage transcriptome during M. tuberculosis infection, activating antimicrobial pathway

70 fter the first and second vaccination, and M tuberculosis infection and disease were assessed at the

71 inatory power between different states of M. tuberculosis infection and disease.

72 Variation in the outcome of tuberculosis infection and diseases has been attributed

73 on CD4(+) and CD8(+) T-cell responses to M. tuberculosis infection and examine the roles of distinct

74 ence factor and macrophages are critical for tuberculosis infection and immunity, we studied ESAT-6 s

75 host genetically heterogeneous Mycobacterium tuberculosis infection and its effect on treatment respo

76 ne responses needed to control Mycobacterium tuberculosis infection and may affect responses to live

77 Recent findings from studies of tuberculosis infection and of patients with Mendelian pr

78 e macaque model are translatable to human M. tuberculosis infection and offer important insights into

79 The form of tuberculosis infection and presence of HIV seemed not to

80 itical bactericidal cells and targets for M. tuberculosis infection and proliferation throughout the

81 ation of biomarkers for latent Mycobacterium tuberculosis infection and risk of progression to tuberc

82 entified in people with latent Mycobacterium tuberculosis infection and treated patients with tubercu

83 lar lavage (BAL) from persons with latent M. tuberculosis infection and untreated HIV coinfection wit

84 dominant host cell during early pulmonary M. tuberculosis infection and, therefore, represent attract

85 can be missed during evaluations for latent tuberculosis infection, and can manifest with symptoms d

86 subsets in control of de novo and latent M. tuberculosis infection, and in the evolution of T-cell i

87 every 1000 people globally carry latent MDR tuberculosis infection, and prevalence is around ten tim

88 erate vaccine-induced T-cell responses on M. tuberculosis infection, and provide insights to overcome

89 eading to immune containment early during M. tuberculosis infection, and support the idea that import

90 nce than children with a negative result for tuberculosis infection, and this incidence was greatest

91 inflammation is a hallmark of Mycobacterium tuberculosis infection, and understanding how this is re

92 ials of vitamin D supplementation to prevent tuberculosis infection are lacking.

93 he mechanisms by which IFN-gamma controls M. tuberculosis infection are only partially understood.

94 o migrate into the lung during Mycobacterium tuberculosis infection are unknown.

95 an effective adaptive immune response to M. tuberculosis infection are yet to be defined.

96 cated on the assumption that most paediatric tuberculosis infections are acquired within the househol

97 nce that suggests BCG may protect against M. tuberculosis infection as well as disease.

98 The secondary outcome was the prevalence of tuberculosis infection, as assessed by an interferon gam

99 sanroque mice showed enhanced control of M. tuberculosis infection associated with delayed bacterial

100 Patients were tested for Mycobacterium tuberculosis infection at baseline with commercially ava

101 ediator of IFN-gamma-dependent control of M. tuberculosis infection both in vitro and in vivo.

102 n exhibited significantly lower levels of M. tuberculosis infection burdens in lung lobes and extrapu

103 rofiles compared to those who develop latent tuberculosis infection but prior to any signs of infecti

104 Mycobacterium tuberculosis infections cause 9 million new tuberculosis

105 M. tuberculosis infection caused a significant degree of mo

106 Mycobacterium tuberculosis infection causes high rates of morbidity an

107 cter co-infection, (2) aerosol Mycobacterium tuberculosis infection changes the gut microbiota, (3) o

108 meningitis (TBM) is the most lethal form of tuberculosis infection, characterized by a dysregulated

109 us macaque (Macaca fascicularis) model of M. tuberculosis infection closely mirrors the infection out

110 on in lung bacterial loads during chronic M. tuberculosis infection compared with fully IL-10-compete

111 Given the estimated prevalence of latent tuberculosis infection, compared with the limited testin

112 ved that exosomes released during a mouse M. tuberculosis infection contribute significantly to its T

113 sed risk of tuberculosis infection; however, tuberculosis infection control (TBIC) measures are often

114 adherence support, complemented by universal tuberculosis infection control measures in healthcare fa

115 transmission by universal implementation of tuberculosis infection control measures should be priori

116 e identification of effective strategies for tuberculosis infection control, improved understanding o

117 timulated gene (ISG) expression following M. tuberculosis infection, cytosolic nucleic acid transfect

118 nrolled adults 18 to 50 years of age with M. tuberculosis infection (defined by positive results on i

119 fungal diseases into existing HIV infection, tuberculosis infection, diabetes, chronic respiratory di

120 The presence of tuberculosis infection did not predict incident disease

121 h M tuberculosis or reactivation of latent M tuberculosis infection during such treatment.

122 luding: (1) preventing progression of latent tuberculosis infection, especially in women coinfected w

123 t weeks 1 and 3 after high-dose (500 CFU) M. tuberculosis infection exhibited significantly lower lev

124 reventive therapy with a positive result for tuberculosis infection had significantly higher 2-year c

125 nduces sterilizing immunity to Mycobacterium tuberculosis infection has been elusive.

126 proinflammatory cytokines in controlling M. tuberculosis infection has been established, the effects

127 changes immediately following Mycobacterium tuberculosis infection have not been evaluated.

128 I, whose potential roles in resistance to M. tuberculosis infection have not yet been investigated.

129 rculosis prevalence are at increased risk of tuberculosis infection; however, tuberculosis infection

130 ost resistance against chronic Mycobacterium tuberculosis infection; however, which cell types are ke

131 underline the necessity of addressing latent tuberculosis infection if further progress is to be made

132 Furthermore, during M. tuberculosis infection, Il10 expression in CD4(+) T cell

133 een shown to dampen Th1 cell responses to M. tuberculosis infection impairing bacterial clearance.

134 nd previously reported genes associated with tuberculosis infection in a cohort with longitudinal mea

135 The estimated incidence of M. tuberculosis infection in adults was 1.5-6 times higher

136 e associated with decreased prevalence of M. tuberculosis infection in adults.

137 We modeled the incidence of M. tuberculosis infection in all age groups using these con

138 ess, scale-up of targeted testing for latent tuberculosis infection in at-risk populations, scale-up

139 Our study confirms the presence of M. tuberculosis infection in cattle in India, sequencing of

140 s and the main wildlife reservoir for bovine tuberculosis infection in cattle.

141 rns, as well as the observed incidence of M. tuberculosis infection in children and the prevalence of

142 The prevalence of tuberculosis infection in children born in 2012 was 3.3%

143 ognition that the diagnosis and treatment of tuberculosis infection in children is a necessary compon

144 sation and discovery of novel treatments for tuberculosis infection in children should account for me

145 pears to reduce acquisition of Mycobacterium tuberculosis infection in children, measured using inter

146 ice, compromises their ability to control M. tuberculosis infection in extrapulmonary organs.

147 he importance of strategies to target latent tuberculosis infection in high risk populations and thus

148 r receptor, pregnane X receptor (PXR), in M. tuberculosis infection in human monocyte-derived macroph

149 Mycobacterium tuberculosis infection in humans triggers formation of g

150 lost their ability to enhance control of M. tuberculosis infection in infected macrophages.

151 bsequently mediate the failure to control M. tuberculosis infection in macrophages.

152 r cell-derived macrophages and attenuated M. tuberculosis infection in mice (with ~8-fold bacterial l

153 We previously showed that M. tuberculosis infection in mice induces expression of the

154 ietic cells in resistance against chronic M. tuberculosis infection in mice infected with M. tubercul

155 cell-derived macrophages, and attenuated M. tuberculosis infection in mice.

156 ibodies attenuates severity of Mycobacterium tuberculosis infection in mice.

157 could protect against aerosol Mycobacterium tuberculosis infection in mice.

158 cobacterium tuberculosis (Mtb) causes latent tuberculosis infection in one-third of the world populat

159 Children are rarely diagnosed with tuberculosis infection in routine care in international

160 may confer protection against Mycobacterium tuberculosis infection in the absence of IFN-gamma signa

161 en injected into healthy mice, caused active tuberculosis infection in the animal's lung.

162 arly innate immune response to Mycobacterium tuberculosis infection in the lung.

163 nate immune protection in early stages of M. tuberculosis infection in the lung.

164 , conferred equivalent protection against M. tuberculosis infection in the lungs of Rag(-/-) mice whe

165 ly isoniazid and rifapentine to treat latent tuberculosis infection in the United States, and such tr

166 ma is essential for control of Mycobacterium tuberculosis infection in vitro and in vivo.

167 etabolic program essential for control of M. tuberculosis infection in vitro and in vivo.

168 phagy factor that has been studied during M. tuberculosis infection in vivo and autophagy-independent

169 bacterial persisters, and rapidly cleared M. tuberculosis infection in vivo.

170 equirement for autophagy in resistance to M. tuberculosis infection in vivo.

171 xamined clinical cohorts of active pulmonary tuberculosis infection in whole blood.

172 Accurate estimates of Mycobacterium tuberculosis infection in young children provide a criti

173 hought to be involved in establishing latent tuberculosis infections in response to hypoxia and nitri

174 acrophage activation by type I IFN during M. tuberculosis infection, in the absence of IFN-gamma sign

175 ming of clinical disease after Mycobacterium tuberculosis infection; incident disease can result from

176 We discovered that M. tuberculosis infection increases the expression of macro

177 M. tuberculosis infection induced a shift from oxidative ph

178 actor for transition of latent Mycobacterium tuberculosis infection into active tuberculosis (TB).

179 The negative predictive value of REFtb for tuberculosis infection is 93%, and the positive predicti

180 Reactivation of latent Mycobacterium tuberculosis infection is an important health concern fo

181 idence suggests the outcome of Mycobacterium tuberculosis infection is established rapidly after expo

182 ially in settings where the prevalence of M. tuberculosis infection is low and environmental sensitiz

183 for, and treatment of, latent Mycobacterium tuberculosis infection is routine before initiation of a

184 critical cellular source of IL-10 during M. tuberculosis infection is still unknown.

185 involved in protecting against Mycobacterium tuberculosis infection is urgently needed to inform stra

186 Tuberculosis (TB), caused by Mycobacterium tuberculosis infection, is a leading cause of mortality

187 lveolar lavage cells from donors with latent tuberculosis infection limited the growth of virulent My

188 proach, we show that individuals with latent tuberculosis infection (Ltb) and active tuberculosis dis

189 Predictors of latent tuberculosis infection (LTBI) among close contacts of pe

190 tor for reactivation of latent Mycobacterium tuberculosis infection (LTBI) and progression to active

191 Persons at high risk of latent tuberculosis infection (LTBI) and/or progression to tube

192 Pregnant women with latent tuberculosis infection (LTBI) are at high risk for devel

193 enal transplant candidates (RTC) with latent tuberculosis infection (LTBI) are at significant risk fo

194 oninferiority trials of treatment for latent tuberculosis infection (LTBI) are challenging because of

195 d and remotely acquired latent Mycobacterium tuberculosis infection (LTBI) are clinically indistingui

196 The tests for diagnosing latent tuberculosis infection (LTBI) are limited by a poor pred

197 om 74 individuals presumed to have latent M. tuberculosis infection (LTBI) based on close contact wit

198 d TB reactivation in individuals with latent tuberculosis infection (LTBI) coinfected with HIV.

199 uberculosis (Mtb) during asymptomatic latent tuberculosis infection (LTBI) in humans is currently lac

200 The prevalence and incidence of latent tuberculosis infection (LTBI) in patients with kidney tr

201 noncompletion of treatment (NCT) for latent tuberculosis infection (LTBI) in the PREVENT TB trial we

202 geted testing and treatment (TTT) for latent tuberculosis infection (LTBI) is a recommended strategy

203 Treatment of latent tuberculosis infection (LTBI) is an important component

204 Treatment of latent tuberculosis infection (LTBI) is important for tuberculo

205 While this latent tuberculosis infection (LTBI) is not contagious, reactiv

206 flammatory responses used to identify latent tuberculosis infection (LTBI) lose positivity during pre

207 ulosis before entry to the UK and for latent tuberculosis infection (LTBI) post-entry for reduction o

208 ve to ten percent of individuals with latent tuberculosis infection (LTBI) progress to active tubercu

209 Efforts to expand treatment of latent tuberculosis infection (LTBI) raise concerns for missed

210 the association between diabetes and latent tuberculosis infection (LTBI) remains limited and incons

211 Latent tuberculosis infection (LTBI) screening and treatment is

212 Latent tuberculosis infection (LTBI) test discordance is poorly

213 d for predicting the progression from latent tuberculosis infection (LTBI) to ATB.

214 s the identification and treatment of latent tuberculosis infection (LTBI) to prevent progression to

215 apy is associated with progression of latent tuberculosis infection (LTBI) to tuberculosis (TB) disea

216 Increased risk of progression from latent tuberculosis infection (LTBI) to tuberculosis (TB) disea

217 eptance and compliance with available latent tuberculosis infection (LTBI) treatment regimens has bee

218 SIV adults, 14.4% were diagnosed with latent tuberculosis infection (LTBI), 63.5% were susceptible to

219 among individuals with latent Mycobacterium tuberculosis infection (LTBI), but validated estimates o

220 h the aim to improve the detection of latent tuberculosis infection (LTBI), especially among recently

221 scar or vaccination history, against latent tuberculosis infection (LTBI), measured via IGRA, was as

222 d-Plus (QFT-Plus) for diagnosis of latent M. tuberculosis infection (LTBI).

223 based tests intended for diagnosis of latent tuberculosis infection (LTBI).

224 ty in susceptibility to latent Mycobacterium tuberculosis infection (LTBI).

225 o influence T and B cell responses in latent tuberculosis infection (LTBI).

226 (ATB) from healthy controls (HC) and latent tuberculosis infections (LTBI).

227 have no clinical evidence of disease (latent tuberculosis infection [LTBI]).

228 Thus, induction of HO1 by M. tuberculosis infection may be a mycobacterial virulence

229 and 133 [51%] of 263 individuals for latent tuberculosis infection), mental health (eg, highest repo

230 course rifapentine-based regimens for latent tuberculosis infection.Methods: Rifapentine pharmacokine

231 iciency of histopathology analysis for mouse tuberculosis infection models, this approach has also br

232 Further, mice deficient in HO1 succumb to M. tuberculosis infection more readily than do wild-type mi

233 o-date knowledge in three areas of childhood tuberculosis infection-namely, pathophysiology, diagnosi

234 end the global tuberculosis epidemic, latent tuberculosis infection needs to be addressed.

235 d the choice of treatment regimen for latent tuberculosis infection.Objectives: To evaluate the effec

236 frequency (MAF) = 40.2%), associated with M. tuberculosis infection (odds ratio (OR) = 1.14, P = 3.1

237 M. tuberculosis infection of IFN-gamma-activated macrophage

238 The pathway of regulation involves M. tuberculosis infection of macrophages and suppression of

239 Here we show that Mycobacterium tuberculosis infection of macrophages induces IL-36gamma

240 erated during host immune responses after M. tuberculosis infection of macrophages.

241 M. tuberculosis infection of primary human monocytes increa

242 tomic profiles of individuals with latent M. tuberculosis infection or tuberculosis.

243 (MAF = 19.1%, rs9272785), associated with M. tuberculosis infection (P = 9.3 x 10(-9), OR = 1.14).

244 e results highlight the dynamic nature of M. tuberculosis infection, population structure and resista

245 obiological features and clinical mimicry of tuberculosis infection pose diagnostic challenges in hig

246 ates of tuberculosis disease incidence and M tuberculosis infection prevalence.

247 shrink the reservoir of latent Mycobacterium tuberculosis infection (preventive therapy), shorten the

248 tes (T2D) have a lower risk of Mycobacterium tuberculosis infection, progression from infection to tu

249 ndations about diagnostic testing for latent tuberculosis infection, pulmonary tuberculosis, and extr

250 The fourth-generation QuantiFERON test for tuberculosis infection, QuantiFERON-TB Gold Plus (QFT-Pl

251 , but additional mechanisms of control of M. tuberculosis infection remain to be identified.

252 regions of the world in which Mycobacterium tuberculosis infection remains endemic and vaccination a

253 autophagy, how human macrophages control M. tuberculosis infection remains less well understood.

254 s (Abs) in the defense against Mycobacterium tuberculosis infection remains uncertain.

255 trophil recruitment and activation during M. tuberculosis infection, representing a novel biological

256 iciency virus-induced reactivation of latent tuberculosis infection results in an increased expressio

257 ambia who never develop latent Mycobacterium tuberculosis infection shows distinct transcriptomic, an

258 (age, region), and clinical attributes (HIV, tuberculosis infection status, previous tuberculosis); a

259 f 0.001-0.01%, and this did not differ by M. tuberculosis infection status.

260 illance pathway in response to Mycobacterium tuberculosis infection stimulates ubiquitin-dependent au

261 of participants harbored a heterogeneous M. tuberculosis infection; such heterogeneity was independe

262 of hypoxic stress and in a mouse model of M. tuberculosis infection, suggesting that the pathogen req

263 ata specific to Indian children and incident tuberculosis infection (TBI) exist.

264 Completion of treatment for tuberculosis infection (TBI) with 9 months of self-admin

265 nding preventive therapy use must decide how tuberculosis infection testing should be used for risk s

266 ore people die every year from Mycobacterium tuberculosis infection than from infection by any other

267 n of Th1 cell input into the lungs during M. tuberculosis infection that is regulated by chemokine re

268 me1), is highly induced during Mycobacterium tuberculosis infection that orchestrates immune evasion

269 effective for the treatment of Mycobacterium tuberculosis infections that no longer respond to conven

270 rd assessments of interaction between latent tuberculosis infection, the HIV serostatus of index case

271 his article that during the first 14 d of M. tuberculosis infection, the predominant cells expressing

272 ars are at high risk of progressing first to tuberculosis infection, then to tuberculosis disease and

273 ed by a period of asymptomatic Mycobacterium tuberculosis infection; therefore, identifying infected

274 Among individuals with latent M. tuberculosis infection, those with DM had diminished fre

275 h mouse macrophages control intracellular M. tuberculosis infection through several mechanisms, such

276 or predicting progression from Mycobacterium tuberculosis infection to active disease is unknown.

277 model of T-cell transfer and aerosolized M. tuberculosis infection to assess the contributions of TN

278 global burden of multidrug-resistant latent tuberculosis infection to inform tuberculosis eliminatio

279 ctively predict progression of Mycobacterium tuberculosis infection to tuberculosis disease might lea

280 After M. tuberculosis infection, TOLLIP-deficient monocytes demon

281 e reactivation risk, and even shorter latent tuberculosis infection treatment regimens than currently

282 re in international settings and few receive tuberculosis infection treatment.

283 ementation did not result in a lower risk of tuberculosis infection, tuberculosis disease, or acute r

284 h immunodeficiency, as well as Mycobacterium tuberculosis infection, underscoring their importance in

285 nd exacerbate pathology during Mycobacterium tuberculosis infection upon GM-CSF blockade.

286 capitulates all clinical aspects of human M. tuberculosis infection, using a human microarray and ana

287 he role of IL-21R signaling in Mycobacterium tuberculosis infection, using IL-21R knockout (KO) mice.

288 hed for and included studies in which latent tuberculosis infection was assessed in 2 groups: childre

289 Latent tuberculosis infection was found in 577 of 878 (65.7%) a

290 Latent tuberculosis infection was measured through tuberculin s

291 Protection against M. tuberculosis infection was strongly associated with BCG

292 on CD8(+) T-cell responses during latent M. tuberculosis infection, we estimated the cytokine and cy

293 n in vitro macrophage model of Mycobacterium tuberculosis infection, we identified several experiment

294 rom 97 US immigrants at various stages of M. tuberculosis infection, we showed protective in vitro an

295 inflammatory disease caused by Mycobacterium tuberculosis infection which causes tremendous morbidity

296 or (TNF) is crucial to control Mycobacterium tuberculosis infection, which remains a leading cause of

297 ession pattern in individuals with latent M. tuberculosis infection with DM and those with latent M.

298 s, including those with latent and active M. tuberculosis infection, with or without concomitant HIV

299 s infection with DM and those with latent M. tuberculosis infection without DM.

300 we investigated whether host immunity to M. tuberculosis infection would be modulated in mice with c