ライフサイエンスコーパス: tuberculosis infection

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

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

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

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

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

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

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

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

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

10 nize and inhibit intracellular Mycobacterium tuberculosis infection.

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

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

13 variability in the response to Mycobacterium tuberculosis infection.

14 lung granulomas of animals exhibiting latent tuberculosis infection.

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

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

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

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

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

20 egral part of the host immune response to M. tuberculosis infection.

21 s well as successfully treated Mycobacterium tuberculosis infection.

22 host-pathogen interactions in Mycobacterium tuberculosis infection.

23 ined as having tuberculosis due to recent M. tuberculosis infection.

24 rial burdens and increased mortality upon M. tuberculosis infection.

25 to effective adaptive immune responses to M. tuberculosis infection.

26 t cGAS is a vital innate immune sensor of M. tuberculosis infection.

27 to have in vivo activity in murine models of tuberculosis infection.

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

29 is important for resistance to Mycobacterium tuberculosis infection.

30 s the pathological hallmark of Mycobacterium tuberculosis infection.

31 and host response-independent markers of M. tuberculosis infection.

32 gen-specific CD4(+) T cells responding to M. tuberculosis infection.

33 ially to the overall IFN-beta response to M. tuberculosis infection.

34 ure, and progression of latent Mycobacterium tuberculosis infection.

35 n promote resistance to lethal Mycobacterium tuberculosis infection.

36 uberculosis due to reactivation of latent M. tuberculosis infection.

37 rferon impedes the protective response to M. tuberculosis infection.

38 ce in our understanding of the physiology of tuberculosis infection.

39 on-gamma release assays are used to diagnose tuberculosis infection.

40 lation status of macrophage proteins upon M. tuberculosis infection.

41 has a limited role in the pathogenesis of M. tuberculosis infection.

42 with that of WT mice following high-dose M. tuberculosis infection.

43 Granulomas are the hallmark of Mycobacterium tuberculosis infection.

44 2 cells and Tregs are highly resistant to M. tuberculosis infection.

45 virus infection can have before or during M. tuberculosis infection.

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

47 in 17 consecutive SOT candidates with latent tuberculosis infection.

48 diseases other than tuberculosis, or latent tuberculosis infection.

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

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

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

52 -cell responses and susceptibility to latent tuberculosis infection.

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

54 rotection in a murine model of Mycobacterium tuberculosis infection.

55 8 years) recommended for treatment of latent tuberculosis infection.

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

57 rom 22 individuals with latent Mycobacterium tuberculosis infection.

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

59 e complication associated with Mycobacterium tuberculosis infection.

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

61 ated with increased susceptibility to latent tuberculosis infection.

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

63 among individuals with latent Mycobacterium tuberculosis infection.

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

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

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

67 challenge for the treatment of Mycobacterium tuberculosis infections.

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

69 Most tuberculosis infections (84%) were estimated to occur ou

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

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

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

73 Latent tuberculosis infection affects one third of the world's

74 Fluoroquinolone (FQN) therapy of latent tuberculosis infection among contacts of individuals wit

75 We found a reduced risk of tuberculosis infection among the household contacts of p

76 s associated with mixed-strain Mycobacterium tuberculosis infections among patients at high risk for

77 are crucial to the control of Mycobacterium tuberculosis infection and are a key component of curren

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

79 y and vaccine efficacy against Mycobacterium tuberculosis infection and disease, assessed in the per-

80 ts of 3,446 index patients were assessed for tuberculosis infection and disease.

81 tte smoking renders a patient susceptible to tuberculosis infection and disease.

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

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

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

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

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

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

88 advanced (prelethal) stage of Mycobacterium tuberculosis infection and represent a heterogeneous pop

89 air pollution PM may increase the risk of M. tuberculosis infection and the development of TB.

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

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

92 on between immunodominance during primary M. tuberculosis infection and vaccine efficacy, confirming

93 resistance to Mycobacterium bovis BCG and M. tuberculosis infections and to investigate whether TNF i

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

95 In China, the prevalence of latent tuberculosis infection, and preventive interventions aga

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

97 ression that was reduced after Mycobacterium tuberculosis infection, and rs10956514 was associated wi

98 cells were the main source of CXCL5 upon M. tuberculosis infection, and secretion of CXCL5 was reduc

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

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

101 thways have a role in the pathogenesis of M. tuberculosis infections, and ETA or ETB receptor signali

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

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

104 s both at an increased risk for acquiring M. tuberculosis infections as well as at an increased risk

105 r studying the pathogenesis of Mycobacterium tuberculosis infection, as well as for testing the effic

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

107 370 patients with tuberculosis had mixed M. tuberculosis infections, based on 24-locus mycobacterial

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

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

110 re critical for containment of Mycobacterium tuberculosis infection, but little else is known about t

111 bacterial killing in a mouse model of acute tuberculosis infection, but not in a chronic infection m

112 iRNAs in primary human macrophages during M. tuberculosis infection by NanoString and confirmed our f

113 ct of il12rb1 that promotes resistance to M. tuberculosis infection by potentiating T(H) cells respon

114 lusters) were considered to represent recent tuberculosis infection (cases).

115 Mycobacterium tuberculosis infections cause 9 million new tuberculosis

116 K-like (perforin production) responses to M. tuberculosis infection, CD4 depletion abrogated these Th

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

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

119 acking TNFRp75 exhibit greater control of M. tuberculosis infection compared with WT mice.

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

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

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

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

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

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

126 urther understand the biology of subclinical tuberculosis infections, develop novel diagnostics and d

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

128 The presence of tuberculosis infection did not predict incident disease

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

130 egy for treatment of pulmonary Mycobacterium tuberculosis infections, especially those caused by drug

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

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

133 e of B cells and humoral immune responses in tuberculosis infection has been regarded as inferior to

134 ution of IL12Rbeta1DeltaTM to controlling M. tuberculosis infection has not been tested.

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

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

137 fected individuals with latent Mycobacterium tuberculosis infection have substantially higher rates o

138 though its influence on latent Mycobacterium tuberculosis infection (hereafter, "latent infection") r

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

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

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

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

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

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

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

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

147 sis factor (TNF) are necessary to control M. tuberculosis infection in both humans and unvaccinated e

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

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

150 el the emerging comorbidity of Mycobacterium tuberculosis infection in diabetic patients.

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

152 daily isoniazid for 9 months (9H) for latent tuberculosis infection in high-risk persons, but there h

153 eventive therapies cure latent Mycobacterium tuberculosis infection in HIV-infected individuals in hi

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

155 Mycobacterium tuberculosis infection in humans triggers formation of g

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

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

158 al mitogen and differentiation factor, on M. tuberculosis infection in mice was tested in prophylaxis

159 ibodies attenuates severity of Mycobacterium tuberculosis infection in mice.

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

161 nsitive than the TST for diagnosis of latent tuberculosis infection in patients on hemodialysis while

162 onth INH regimen for the treatment of latent tuberculosis infection in solid-organ transplant (SOT) c

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

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

165 ccuracy of these tests in determining latent tuberculosis infection in the hemodialysis population.

166 TSPOT.TB with regards to determining latent tuberculosis infection in the hemodialysis population.

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

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

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

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

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

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

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

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

175 In 2010, the median number of Mycobacterium tuberculosis infections in children was 7,591,759 (5,800

176 screening and preventive therapy for latent tuberculosis infections in individuals with diabetes.

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

178 or control of Mycobacterium tuberculosis (M. tuberculosis) infection in humans.

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

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

181 M. tuberculosis infection induced a shift from oxidative ph

182 ent of individuals with latent Mycobacterium tuberculosis infection is an essential component of tube

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

184 st protective immunity against Mycobacterium tuberculosis infection is critically dependent on the in

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

186 entine and isoniazid for treatment of latent tuberculosis infection is safe and effective for persons

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

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

189 For mice with a well established M. tuberculosis infection, KGF given every 3 days beginning

190 of mice to influenza A virus, followed by M. tuberculosis infection, leads to enhanced mycobacterial

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

192 ispensable in alveolar macrophages during M. tuberculosis infection, loss of Atg5 in PMNs can sensiti

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

194 We compared the prevalence of latent tuberculosis infection (LTBI) among persons who had rece

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

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

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

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

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

200 Current guidelines limit latent tuberculosis infection (LTBI) evaluation to persons in t

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

202 Effective treatment of latent tuberculosis infection (LTBI) is an important component

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

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

205 Screening and therapy of latent tuberculosis infection (LTBI) is recommended in solid or

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

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

208 In latent tuberculosis infection (LTBI) spread of the bacteria is

209 Latent tuberculosis infection (LTBI) test discordance is poorly

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

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

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

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

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

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

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

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

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

219 ed a role for two miRNAs upregulated upon M. tuberculosis infection, miR-132 and miR-26a, as negative

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

221 Delayed adaptive responses, a hallmark of M. tuberculosis infection, not only lead to persistence but

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

223 We showed that pulmonary M. tuberculosis infection of CD4-depleted macaques surprisi

224 M. tuberculosis infection of diabetic guinea pigs resulted

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

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

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

228 nd to prevent rapid TB progression during M. tuberculosis infection of nonhuman primates.

229 M. tuberculosis infection of primary human monocytes increa

230 Finding immunometabolic changes during M. tuberculosis infection opens the way to new strategies f

231 However, we detected no efficacy against M tuberculosis infection or disease, although the study wa

232 Absence of prior M. tuberculosis infection or sensitization with environment

233 th one of three standard regimens for latent tuberculosis infection or tumor necrosis factor (TNF)-ne

234 tic choriomeningitis virus and Mycobacterium tuberculosis infections or solid tumors.

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

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

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

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

239 nfected murine lung tissue and found that M. tuberculosis infection promotes upregulation of Cxcr2 an

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

241 g the sterilizing activities of human latent tuberculosis infection regimens.

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

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

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

245 di-AMP-mediated IFN-beta induction during M. tuberculosis infection requires stimulator of interferon

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

247 understanding of the role of ATG5 during M. tuberculosis infection, reveal new outcomes of ATG5 acti

248 CD4 depletion during M. tuberculosis infection revealed the ability of CD8(+) T

249 The billions of people with latent tuberculosis infection serve as the seedbeds for future

250 Clinical suspicion of mixed M. tuberculosis infections should be high for patients with

251 n their functions in host defense against M. tuberculosis infection since their depletion leads to en

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

253 derwent tuberculin skin testing to determine tuberculosis infection status.

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

255 d drug regimens specifically for subclinical tuberculosis infection, strengthen health systems and co

256 age transcriptome profiling revealed that M. tuberculosis infection strongly induced the expression o

257 , statin treatment in experimental murine M. tuberculosis infection studies increased host protection

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

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

260 to sequential peaks in vitamin D deficiency, tuberculosis infection, symptom onset, and diagnosis may

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

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

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

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

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

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

267 Like the host response to M. tuberculosis infections, the host response to these infe

268 vailable to determine the presence of latent tuberculosis infection: the tuberculin skin test (TST),

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

270 tion plays a prominent role in Mycobacterium tuberculosis infection; therefore, to develop new tools

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

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

273 fected host resistance against Mycobacterium tuberculosis infection through the induction of alternat

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

275 Expanded testing and treatment for latent tuberculosis infection to all HIV-infected adults, irres

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

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

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

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

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

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

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

283 Previous tuberculosis infection was diagnosed in 5 of 77 patients

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

285 Latent tuberculosis infection was measured through tuberculin s

286 The resistance of Cxcl5(-/-) mice to M. tuberculosis infection was not due to heightened M. tube

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

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

289 retroviral therapy; participants with latent tuberculosis infection were eligible if they had complet

290 Rates of latent tuberculosis infection were higher for men than women (p

291 rculosis from other diseases and from latent tuberculosis infection were identified from genomewide a

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

293 h nodes and attendant improved control of M. tuberculosis infection, while their presence in the lung

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

295 rculosis-exposed cohabitants were tested for tuberculosis infection with the tuberculin skin test (n

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

297 ing statin therapy were more resistant to M. tuberculosis infection, with reduced bacterial burdens,

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

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

300 h associated with stress survival and latent tuberculosis infection, yet the activities and intracell