ライフサイエンスコーパス: mycobacterial infection

1 l homing and delayed lung recruitment during mycobacterial infection.

2 ical modulation of PTEN signaling can affect mycobacterial infection.

3 rlap between susceptibility loci for IBD and mycobacterial infection.

4 anoid production in vertebrate resistance to mycobacterial infection.

5 estrating the initial neutrophil response to mycobacterial infection.

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

7 the mechanisms underlying susceptibility to mycobacterial infection.

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

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

10 rks of protective immune responses following mycobacterial infection.

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

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

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

14 de variety of clinical conditions, including mycobacterial infection.

15 sphoantigen treatment or phosphoantigen plus mycobacterial infection.

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

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

18 HDAC gene expression was not affected by mycobacterial infection.

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

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

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

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

23 shed model for discovering genes involved in mycobacterial infection.

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

25 be a useful genetically tractable model for mycobacterial infection.

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

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

28 granuloma formation is a hallmark of chronic mycobacterial infection.

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

30 3 yr prior to developing clinically apparent mycobacterial infection.

31 suggests a contributory role in immunity to mycobacterial infection.

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

33 hages become functionally deactivated during mycobacterial infection.

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

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

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

37 responses associated with protection against mycobacterial infection.

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

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

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

41 ntal alterations of host immune responses to mycobacterial infection.

42 crophage cDNA libraries for genes induced by mycobacterial infection.

43 tracellular components and the spread of the mycobacterial infection.

44 ernative cytotoxic pathway to the control of mycobacterial infection.

45 plenic tissues of patients with disseminated mycobacterial infection.

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

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

48 ant component of vascular dysfunction during mycobacterial infection.

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

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

51 sceptibility to disseminated non-tuberculous mycobacterial infection.

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

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

54 E2 signaling to vascular permeability during mycobacterial infection.

55 e important and can affect susceptibility to mycobacterial infection.

56 tment-refractory disseminated nontuberculous mycobacterial infection.

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

58 and mycobacteria for iron acquisition during mycobacterial infection.

59 ne polyendocrine syndrome type 1 and chronic mycobacterial infection.

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

61 are imperative for clearance or survival of mycobacterial infection.

62 lung disease associated with nontuberculous mycobacterial infection.

63 to the thymus that most efficiently control mycobacterial infection.

64 terium tuberculosis and 3 had nontuberculous mycobacterial infection.

65 humans with chronic granulomatous disease to mycobacterial infection.

66 th efforts to develop new antimicrobials for mycobacterial infections.

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

68 ibit therapeutic potential against pulmonary mycobacterial infections.

69 tential routes to novel therapeutics against mycobacterial infections.

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

71 ts or be suitable vaccination candidates for mycobacterial infections.

72 afford alternative lines of defense against mycobacterial infections.

73 associated with disseminated nontuberculous mycobacterial infections.

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

75 ion and limiting growth and dissemination of mycobacterial infections.

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

77 nses are critical for protective immunity to mycobacterial infections.

78 -gamma associated with severe nontuberculous mycobacterial infections.

79 ential for development of new treatments for mycobacterial infections.

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

81 ive transplants before developing refractory mycobacterial infections.

82 s can mount adaptive immune responses during mycobacterial infections.

83 for understanding the pathogenesis of other mycobacterial infections.

84 unity and necessary for efficient control of mycobacterial infections.

85 opportunities for preventing and controlling mycobacterial infections.

86 cells may contribute to adaptive immunity to mycobacterial infections.

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

88 gnaling pathways responsible for controlling mycobacterial infections.

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

90 ffector functions are essential for clearing mycobacterial infections.

91 associated with disseminated nontuberculous mycobacterial infections.

92 es further investigation in the treatment of mycobacterial infections.

93 mma R1) who have disseminated nontuberculous mycobacterial infections.

94 their chronic intake increases the risk for mycobacterial infections.

95 ith immunosuppressive disorders that lead to mycobacterial infections.

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

97 warts and 3 had disseminated nontuberculous mycobacterial infections.

98 e against infections, including experimental mycobacterial infections.

99 lying localised and systemic non-tuberculous mycobacterial infections.

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

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

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

103 stigated as components of novel vaccines for mycobacterial infections.

104 uctive pulmonary disease, and nontuberculous mycobacterial infections.

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

106 d participating in the immunopathogenesis of mycobacterial infections.

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

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

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

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

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

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

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

114 Mycobacterial infection and host-derived oxidized phosph

115 Both mycobacterial infection and immunization with Mtb lipids

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

139 Mycobacterial infections are critically controlled by in

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

141 Tuberculosis and other mycobacterial infections are the most serious infectious

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

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

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

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

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

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

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

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

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

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

152 Nontuberculous mycobacterial infections caused by Mycobacterium abscess

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

154 Upon mycobacterial infection, Clec4b1-deficient mice showed r

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

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

157 Nontuberculous mycobacterial infections due to autoantibodies targeting

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

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

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

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

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

163 Thus, during mycobacterial infection, granuloma macrophages are broad

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

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

166 Mycobacterial infection has been implicated as a possibl

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

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

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

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

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

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

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

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

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

176 Mycobacterial infection in humans and zebrafish results

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 The possibility that mycobacterial infections induce variant cytokine mRNA en

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

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

203 Mycobacterial infection inhibited IFN-gamma-induced expr

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

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

206 Protective immunity to mycobacterial infection is incompletely understood but p

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

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

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

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

211 During mycobacterial infection, macrophages with lysosomal stor

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

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

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

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

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

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

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

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

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

221 Ocular mycobacterial infection occurs in nonendemic areas and c

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

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

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

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

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

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

228 Thus, mycobacterial infections of macaques induced variant mRN

229 Mycobacterial infections of macrophages have been shown

230 In mycobacterial infections of other species, gammadelta T

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

232 Secondary mycobacterial infection on day 14 after primary BCG chal

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

234 However, mycobacterial infection or TLR2 stimulation up-regulated

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

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

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

238 Although mycobacterial infection potently induces mTOR activity,

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

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

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

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

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

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

245 Host defense against mycobacterial infection requires the participation of mo

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

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

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

249 Nontuberculous mycobacterial infections should be considered in the dif

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

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

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

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

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

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

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

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

258 During pulmonary mycobacterial infection, there is increased trafficking

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 Cryptococcal and nontuberculous mycobacterial infections were the major presenting oppor

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

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

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

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