ライフサイエンスコーパス: mycobacterial infection

1 complex granulomas that are the hallmark of mycobacterial infection.

2 are imperative for clearance or survival of mycobacterial infection.

3 lung disease associated with nontuberculous mycobacterial infection.

4 to the thymus that most efficiently control mycobacterial infection.

5 terium tuberculosis and 3 had nontuberculous mycobacterial infection.

6 humans with chronic granulomatous disease to mycobacterial infection.

7 l homing and delayed lung recruitment during mycobacterial infection.

8 ical modulation of PTEN signaling can affect mycobacterial infection.

9 l sites and are known to respond robustly to mycobacterial infection.

10 rlap between susceptibility loci for IBD and mycobacterial infection.

11 anoid production in vertebrate resistance to mycobacterial infection.

12 tion compromises protective host immunity to mycobacterial infection.

13 pulation of AMs that are more susceptible to mycobacterial infection.

14 the mechanisms underlying susceptibility to mycobacterial infection.

15 ty to interplay with Tregs in the context of mycobacterial infection.

16 ied as an important factor in the control of mycobacterial infection.

17 rks of protective immune responses following mycobacterial infection.

18 ecretion and ESAT-6 enhance the virulence of mycobacterial infection.

19 curs in mice singly deficient in Irgm1 after mycobacterial infection.

20 g-specific antimicrobial T-cell responses in mycobacterial infection.

21 de variety of clinical conditions, including mycobacterial infection.

22 sphoantigen treatment or phosphoantigen plus mycobacterial infection.

23 l dissemination characterize severe forms of mycobacterial infection.

24 rs in mediating a macrophage's response to a mycobacterial infection.

25 a macrophage's proinflammatory response to a mycobacterial infection.

26 HDAC gene expression was not affected by mycobacterial infection.

27 is, as well as those needed specifically for mycobacterial infection.

28 TNF-alpha gene expression in the setting of mycobacterial infection.

29 ific Vgamma2Vdelta2(+) T cells during active mycobacterial infection.

30 e fibrosis in the granuloma during a chronic mycobacterial infection.

31 shed model for discovering genes involved in mycobacterial infection.

32 n shown to play a role in protection against mycobacterial infection.

33 be a useful genetically tractable model for mycobacterial infection.

34 d within the lungs of mice that have chronic mycobacterial infection.

35 onal T cell populations can be protective in mycobacterial infection.

36 granuloma formation is a hallmark of chronic mycobacterial infection.

37 s mechanism also operates in the lung during mycobacterial infection.

38 ant component of vascular dysfunction during mycobacterial infection.

39 3 yr prior to developing clinically apparent mycobacterial infection.

40 suggests a contributory role in immunity to mycobacterial infection.

41 ive type 1 cytokine response in persons with mycobacterial infection.

42 hages become functionally deactivated during mycobacterial infection.

43 ve been found to be necessary for control of mycobacterial infection.

44 by which antibody could modify the course of mycobacterial infection.

45 butes to host protection in a mouse model of mycobacterial infection.

46 responses associated with protection against mycobacterial infection.

47 I and class Ia responses are susceptible to mycobacterial infection.

48 for the loss of Mtb-reactive T cells during mycobacterial infection.

49 E2 signaling to vascular permeability during mycobacterial infection.

50 who had a diagnosis of a disease other than mycobacterial infection.

51 ntal alterations of host immune responses to mycobacterial infection.

52 and mycobacteria for iron acquisition during mycobacterial infection.

53 crophage cDNA libraries for genes induced by mycobacterial infection.

54 tracellular components and the spread of the mycobacterial infection.

55 ernative cytotoxic pathway to the control of mycobacterial infection.

56 plenic tissues of patients with disseminated mycobacterial infection.

57 thought to be central to the pathogenesis of mycobacterial infection.

58 in the downregulation of immune response in mycobacterial infection.

59 estrating the initial neutrophil response to mycobacterial infection.

60 s (e.g., interleukin-6 [IL-6] and IL-10), in mycobacterial infection.

61 mited iron conditions, which is critical for mycobacterial infection.

62 ght into the role of host genetic factors in mycobacterial infection.

63 s led to a reassessment of several tenets of mycobacterial infection.

64 sceptibility to disseminated non-tuberculous mycobacterial infection.

65 o play a key role in optimal defense against mycobacterial infection.

66 e that was discovered to be a nontuberculous mycobacterial infection.

67 e important and can affect susceptibility to mycobacterial infection.

68 tment-refractory disseminated nontuberculous mycobacterial infection.

69 e of benefit in the treatment and control of mycobacterial infection.

70 ne polyendocrine syndrome type 1 and chronic mycobacterial infection.

71 re linked to Parkinson's disease, cancer and mycobacterial infection.

72 d participating in the immunopathogenesis of mycobacterial infections.

73 b,d]thiophene-based lead candidates to treat mycobacterial infections.

74 ibit therapeutic potential against pulmonary mycobacterial infections.

75 tential routes to novel therapeutics against mycobacterial infections.

76 ze with antibiotic therapy in the control of mycobacterial infections.

77 ts or be suitable vaccination candidates for mycobacterial infections.

78 afford alternative lines of defense against mycobacterial infections.

79 s a frequent and challenging complication of mycobacterial infections.

80 essential role in a macrophage's response to mycobacterial infections.

81 ion and limiting growth and dissemination of mycobacterial infections.

82 -Guerin (BCG) vaccination to protect against mycobacterial infections.

83 nses are critical for protective immunity to mycobacterial infections.

84 -gamma associated with severe nontuberculous mycobacterial infections.

85 ential for development of new treatments for mycobacterial infections.

86 Nramp1, plays a major role in resistance to mycobacterial infections.

87 ive transplants before developing refractory mycobacterial infections.

88 th efforts to develop new antimicrobials for mycobacterial infections.

89 s can mount adaptive immune responses during mycobacterial infections.

90 for understanding the pathogenesis of other mycobacterial infections.

91 opportunities for preventing and controlling mycobacterial infections.

92 cells may contribute to adaptive immunity to mycobacterial infections.

93 o follow Vgamma2Vdelta2+ T cell responses to mycobacterial infections.

94 ntly been shown to be protective in systemic mycobacterial infections.

95 ffector functions are essential for clearing mycobacterial infections.

96 associated with disseminated nontuberculous mycobacterial infections.

97 es further investigation in the treatment of mycobacterial infections.

98 mma R1) who have disseminated nontuberculous mycobacterial infections.

99 ith immunosuppressive disorders that lead to mycobacterial infections.

100 ays a critical role in host defenses against mycobacterial infections.

101 a useful tool in the clinical management of mycobacterial infections.

102 exhibit important immunological functions in mycobacterial infections.

103 associated with disseminated nontuberculous mycobacterial infections.

104 unity and necessary for efficient control of mycobacterial infections.

105 gnaling pathways responsible for controlling mycobacterial infections.

106 their chronic intake increases the risk for mycobacterial infections.

107 warts and 3 had disseminated nontuberculous mycobacterial infections.

108 e against infections, including experimental mycobacterial infections.

109 lying localised and systemic non-tuberculous mycobacterial infections.

110 se or HIV, might result in predisposition to mycobacterial infections.

111 e potential for the therapeutic treatment of mycobacterial infections.

112 -related infections), tuberculosis and other mycobacterial infections.

113 inst tuberculosis, leprosy, and AIDS-related mycobacterial infections.

114 stigated as components of novel vaccines for mycobacterial infections.

115 uctive pulmonary disease, and nontuberculous mycobacterial infections.

116 des a novel strategy for enhanced control of mycobacterial infections.

117 infections (1.32; 95% CI, 1.30 to 1.34), and mycobacterial infections (1.69; 95% CI, 1.36 to 2.09).

118 Furthermore, we found mycobacterial infection activates host cell Akt phosphor

119 monkeys that developed clinically quiescent mycobacterial infection after BCG inoculation were follo

120 5.10 and 4.65, respectively; both P = .001), mycobacterial infections (AIDS; P = .006), and viral inf

121 Together, our findings demonstrate that mycobacterial infection alters the formation of erythroc

122 hese data suggest that an existing pulmonary mycobacterial infection alters the phenotype of lung den

123 entified a large outbreak of rapidly growing mycobacterial infections among persons who had had footb

124 Mycobacterial infection and accompanying surface TLR act

125 articipate in adaptive immune responses upon mycobacterial infection and could serve as targets for t

126 , we study a patient with recurrent atypical mycobacterial infection and early-onset metastatic bladd

127 lline metabolism for myeloid defense against mycobacterial infection and highlight the potential for

128 Mycobacterial infection and host-derived oxidized phosph

129 Both mycobacterial infection and immunization with Mtb lipids

130 Il-1beta transcription in vivo during early mycobacterial infection and importantly highlight a host

131 binding domain, we identified a patient with mycobacterial infection and myelodysplasia who had an un

132 studied both aerosolized and i.v. models of mycobacterial infection and observed MIF-deficient mice

133 tical function of JAK1 in protection against mycobacterial infection and possibly the immunological s

134 s the importance of lipids in the biology of mycobacterial infection and suggests possible strategies

135 TOR signaling take place concurrently during mycobacterial infection and that host autophagy response

136 opontin augments the host response against a mycobacterial infection and that it acts independently f

137 sential component of resistance to pulmonary mycobacterial infection and that MMP-9, specifically, is

138 ory response when humans are challenged by a mycobacterial infection and that osteopontin contributes

139 host receptors that mediate the detection of mycobacterial infection and the role of individual recep

140 nase A pathways in macrophage signaling upon mycobacterial infection and to show how cAMP production

141 ity of humans with mononuclear cytopenias to mycobacterial infections and highlight the therapeutic p

142 e GPIs in the immunology and pathogenesis of mycobacterial infections and physiology of the organism.

143 p between autophagy, human susceptibility to mycobacterial infections and predisposition loci for inf

144 ctor cells emerged as dominant clones during mycobacterial infections and underwent major recall expa

145 ALB/c and C57BL/6, classically used to study mycobacterial infection, and FVB/N.

146 NQO1 expression was increased after mycobacterial infection, and NQO1 knockdown increased ma

147 umans and livestock were screened for active mycobacterial infection, and opportunistic post-mortem e

148 atency, the cellular and immune responses to mycobacterial infections, and autoimmune diseases such a

149 -gamma is critical in the immune response to mycobacterial infections, and deficits in IFN-gamma prod

150 ive for all six patients with nontuberculous mycobacterial infections, and negative for all 33 patien

151 nction, such as listeriosis, pneumocystosis, mycobacterial infections, and opportunistic fungal and v

152 urs in vivo and that in an in vitro model of mycobacterial infection, apoptosis may be mediated by do

153 The reported outcomes of ocular mycobacterial infection are commonly unfavorable.

154 Furthermore, susceptibilities to mycobacterial infections are caused by metal ion transpo

155 Mycobacterial infections are critically controlled by in

156 potential in pulmonary host defense against mycobacterial infections are poorly defined.

157 Tuberculosis and other mycobacterial infections are the most serious infectious

158 ous granuloma, the central host structure in mycobacterial infection, as well as inflammatory mediato

159 Analysis of Ag-specific CD4(+) T cells in mycobacterial infections at the transcriptome level is i

160 appreciation of the balance required during mycobacterial infection between anti-bacterial activity

161 Neutrophils participate in the control of mycobacterial infection both by directly eliminating bac

162 d on susceptibility to malaria, HIV/AIDS and mycobacterial infection, but other bacterial, viral and

163 xert a major inhibitory effect on control of mycobacterial infection by a mechanism involving the sup

164 crophage deficits increase susceptibility to mycobacterial infection by accelerating granuloma necros

165 that Rev-erbalpha bestows protection against mycobacterial infection by direct gene repression of IL1

166 isease, we examined galectin-3 expression in mycobacterial infection by studying leprosy, an intracel

167 , the data suggest that IL-10 helps maintain mycobacterial infections by acting primarily at the leve

168 Nontuberculous mycobacterial infections caused by Mycobacterium abscess

169 Interestingly, during peak mycobacterial infection, CD11c(hi) MHC(hi) lung DCs had

170 Upon mycobacterial infection, Clec4b1-deficient mice showed r

171 U.S. patients with pulmonary nontuberculous mycobacterial infections, compared them to 30 globally d

172 ion factor GATA2 underlies monocytopenia and mycobacterial infections; dendritic cell, monocyte, B, a

173 Recently, we have found that mycobacterial infection downregulated miR-148a-3p (now t

174 Nontuberculous mycobacterial infections due to autoantibodies targeting

175 me/acute myeloid leukemia, monocytopenia and mycobacterial infections, Emberger syndrome, and dendrit

176 associated with disseminated nontuberculous mycobacterial infection emphasizes the critical role tha

177 cking endogenous CD46 signaling 3 days after mycobacterial infection enhanced BCG-specific T cell res

178 mmatory lipoxins are host detrimental during mycobacterial infections, excess pro-inflammatory lipids

179 her disseminated or pulmonary nontuberculous mycobacterial infections for whom no molecular defect wa

180 Thus, during mycobacterial infection, granuloma macrophages are broad

181 d, rapidly or slowly growing, nontuberculous mycobacterial infection (group 1); 45 patients with anot

182 ic infection, with or without nontuberculous mycobacterial infection (group 2); 9 patients with disse

183 Mycobacterial infection has been implicated as a possibl

184 thermore, isolated pulmonary non-tuberculous mycobacterial infection has been increasing in prevalenc

185 ron supplementation on the susceptibility to mycobacterial infection have been reported.

186 our understanding of T cell responses during mycobacterial infection; however, we have not yet identi

187 hile TNF-deficient mice rapidly succumbed to mycobacterial infection, huTNF KI mice survived, control

188 During the course of mycobacterial infections, IFN-gamma-mediated activation

189 s insight into the metabolic consequences of mycobacterial infection, implicating impaired insulin si

190 The source of mycobacterial infection in 15 SIV-inoculated rhesus maca

191 g the improvement of refractory disseminated mycobacterial infection in a CD40L-deficient patient by

192 t homeostasis and consequently resistance to mycobacterial infection in Drosophila.

193 Mycobacterial infection in humans and zebrafish results

194 pes, could contribute to the defense against mycobacterial infection in humans.

195 tralizing biologics disrupted the control of mycobacterial infection in huTNF KI mice, leading to an

196 s of the CNS that are suppressed by systemic mycobacterial infection in mice and BCG vaccination in h

197 "ML ratio") was noted to affect outcomes of mycobacterial infection in rabbits.

198 ) DC as a major source of IL-12/23p40 during mycobacterial infection in situ and implicate both solub

199 e water may serve as a significant source of mycobacterial infection in SIV-inoculated macaques and s

200 The sites of mycobacterial infection in the lungs of tuberculosis (TB

201 nown about their immunologic function during mycobacterial infection in the lungs.

202 activated macrophages is believed to control mycobacterial infection in the murine system.

203 portant determinant for the establishment of mycobacterial infection in their hosts.

204 on did not modify the course of experimental mycobacterial infection in these mice.

205 ly regulate protective Th1 responses against mycobacterial infection in vivo and suggest that the inh

206 ion, and regulation of p40 production during mycobacterial infection in vivo has been unclear.

207 mediated target cell death to the control of mycobacterial infection in vivo, mice with a disruption

208 itro, and in adaptive immunity in a model of mycobacterial infection in vivo.

209 ear to be necessary for the early control of mycobacterial infection in vivo.

210 been shown to be important in resistance to mycobacterial infection in vivo.

211 it also accounts for approximately 2% of the mycobacterial infections in AIDS patients.

212 Thus, reactivation of latent mycobacterial infections in HIV-1-infected individuals m

213 nd its deficiency predisposes to more severe mycobacterial infections in mice.

214 nism to account for cutaneous infections and mycobacterial infections in T-cell-deficient patients.

215 Resurgence of mycobacterial infections in the United States has led to

216 In 3 patients with post-HCT IRIS related to mycobacterial infection, in vitro data demonstrate the e

217 s in Mendelian predisposition to more severe mycobacterial infections, including by M. tuberculosis,

218 ) plays a significant role in the control of mycobacterial infections, including Mycobacterium avium

219 The possibility that mycobacterial infections induce variant cytokine mRNA en

220 To analyze the counter-regulatory role of mycobacterial infection-induced IFN-gamma in the CNS on

221 -activated macrophages plays a major role in mycobacterial infection-induced thymic atrophy.

222 Mycobacterial infection inhibited IFN-gamma-induced expr

223 ulated by the cytokine environment, which in mycobacterial infection is a balance of proinflammatory

224 ectin Mincle in lung innate immunity against mycobacterial infection is incompletely defined.

225 Protective immunity to mycobacterial infection is incompletely understood but p

226 These findings indicate that resistance to mycobacterial infection is regulated by multiple MyD88-d

227 rophage proinflammatory response following a mycobacterial infection is regulated by SPK/PI-PLC/PKC a

228 In the human mycobacterial infection leprosy, we found that activatio

229 To examine the role of LRG-47 in control of mycobacterial infection, LRG-47(-/-) and wild-type mice

230 During mycobacterial infection, macrophages with lysosomal stor

231 Antimicrobial killing in mycobacterial infections may be accompanied by (transien

232 own as granulomas, long thought to constrain mycobacterial infection, may instead facilitate its spre

233 t insight into how improved vaccines against mycobacterial infections might be constructed.

234 A2-a disease characterized by nontuberculous mycobacterial infection, monocytopenia, B- and NK-cell d

235 An effective host immune response to mycobacterial infection must control pathogen disseminat

236 immunodeficiency syndromes characterized by mycobacterial infection, myelodysplasia, lymphedema, or

237 We have previously reported that during mycobacterial infection, naive CD4(+) T-cell activation

238 Cultures suggestive of Non-tuberculous mycobacterial infections (NTM) were sub-cultured and cha

239 om the preantibiotic era, analogy with other mycobacterial infections, observations of tuberculosis i

240 Ocular mycobacterial infection occurs in nonendemic areas and c

241 However, in vitro models of mycobacterial infection of human macrophages do not full

242 Thus, mycobacterial infection of human THP-1 cells specificall

243 r, previous work by our group has shown that mycobacterial infection of macrophages naturally induces

244 he apoptotic pathway in an in vitro model of mycobacterial infection of mononuclear phagocytes.

245 h gram-negative organisms is well described, mycobacterial infection of native polycystic kidneys aft

246 Except for atypical mycobacterial infection of the index case, the affected

247 Thus, mycobacterial infections of macaques induced variant mRN

248 Mycobacterial infections of macrophages have been shown

249 In mycobacterial infections of other species, gammadelta T

250 Nontuberculous mycobacterial infections of the skin can be seen in case

251 Secondary mycobacterial infection on day 14 after primary BCG chal

252 ation of blood-borne macrophages at sites of mycobacterial infection or antigen deposition is not ess

253 However, mycobacterial infection or TLR2 stimulation up-regulated

254 a and evaluated the pattern and frequency of mycobacterial infections over twelve calendar months per

255 acterium tuberculosis are key players of the mycobacterial infection pathway.

256 perinatal/childhood infections, or atypical mycobacterial infections play a role in expression of in

257 Although mycobacterial infection potently induces mTOR activity,

258 re, to examine the role of complement in the mycobacterial infection process in vivo, mice deficient

259 Exposure of mice deficient in IFN-gamma to mycobacterial infection produces an immune response char

260 The mouse model of mycobacterial infection provides an excellent tool with

261 of the complexity of the T cell response to mycobacterial infection recently.

262 forming growth factor beta (TGF-beta) during mycobacterial infection, recombinant clones of bacillus

263 Therefore, we suggest that during mycobacterial infection, regulatory neutrophils are inst

264 Host defense against mycobacterial infection requires the participation of mo

265 proceeds unchecked throughout the course of mycobacterial infection, resulting in a transition to ex

266 e acute disease is characterized by systemic mycobacterial infection, severe peritonitis, tissue necr

267 Tuberculosis and atypical mycobacterial infection should be in the differential di

268 Nontuberculous mycobacterial infections should be considered in the dif

269 To evaluate host defense mechanisms against mycobacterial infections, studies investigated whether n

270 mutations in LRRK2 confer susceptibility to mycobacterial infection, suggesting LRRK2 also controls

271 s greater than that of THP-1 cells following mycobacterial infection, suggesting that RPE can serve a

272 N-PI3K-Akt mTOR status and susceptibility to mycobacterial infection suggests that the interaction of

273 Importantly, following in vivo mycobacterial infection, Tg/TLR2(-/-) mice failed to dis

274 Thus, NQO1 is a new host target in mycobacterial infection that could potentially be exploi

275 it susceptibility to disseminated, recurrent mycobacterial infections that are associated with defect

276 In several murine models of mycobacterial infection, the absence of IFN-gamma and/or

277 h IFN-gamma is essential for host control of mycobacterial infection, the mechanisms by which the cyt

278 During pulmonary mycobacterial infection, there is increased trafficking

279 the importance of LAM to the pathogenesis of mycobacterial infection, there is no information availab

280 deficiency, which protects mice from severe mycobacterial infections, thereby laying the foundation

281 cell responses are maintained during chronic mycobacterial infection through the continual production

282 less infiltration of macrophages to sites of mycobacterial infection, thus impairing granuloma develo

283 of APC-produced IL-10 on host resistance to mycobacterial infection, transgenic mice expressing huma

284 In experimental mycobacterial infection, tumor necrosis factor alpha (TN

285 ctor dynamics and responses during pulmonary mycobacterial infection versus acute influenza infection

286 usceptibility to disseminated nontuberculous mycobacterial infections, viral infections, especially w

287 nt tuberculosis, diabetes mellitus, atypical mycobacterial infections, vitamin D deficiency or metabo

288 In one of these, mycobacterial infection was considered to be an importan

289 NF and IL-6 by RP105(-/-) macrophages during mycobacterial infection was not accompanied by diminishe

290 functions in promoting MAPK activation upon mycobacterial infection was not defined in these studies

291 ring the first few weeks following pulmonary mycobacterial infection, we found a drastic increase in

292 that prior silica exposure increases risk of mycobacterial infection, we intratracheally (I.T.) admin

293 s dependent on ERK1/2 activation following a mycobacterial infection, we used RAW 264.7 cells transfe

294 d for the diagnosis of tuberculosis or other mycobacterial infections were tested by a ligase chain r

295 Cryptococcal and nontuberculous mycobacterial infections were the major presenting oppor

296 eutrophils are rapidly recruited to sites of mycobacterial infection, where they phagocytose bacilli.

297 converged downstream pathways in response to mycobacterial infection, which was supported by data ind

298 red cell-autonomous immunity to listerial or mycobacterial infection within macrophages and gene-defi

299 appearance of GCM was due to the presence of mycobacterial infection within the myocardium, and we be

300 We hypothesized that ongoing mycobacterial infection would modulate recruitment and a