ライフサイエンスコーパス: leprosy

1 8 gene were associated with T1R but not with leprosy.

2 CIITA-SOCS1 as new susceptibility genes for leprosy.

3 ost exclusively in patients with lepromatous leprosy.

4 testing was performed on 39 US patients with leprosy.

5 be used as an additional control measure for leprosy.

6 terium leprae challenge in a murine model of leprosy.

7 t with no evidence of active tuberculosis or leprosy.

8 y lead to tools applicable to elimination of leprosy.

9 ing that 248S is a susceptibility factor for leprosy.

10 the mycobacteria that cause tuberculosis or leprosy.

11 ypersensitivity syndrome among patients with leprosy.

12 ion in patients with the progressive form of leprosy.

13 (Th1) inflammatory episode in patients with leprosy.

14 n the genetic control of Crohn's disease and leprosy.

15 rkinson's disease (PD), Crohn's disease, and leprosy.

16 difies susceptibility to Crohn's disease and leprosy.

17 . leprae PGL-1 in initiating nerve damage in leprosy.

18 ohn disease, psoriasis, alopecia areata, and leprosy.

19 that cause diseases such as tuberculosis and leprosy.

20 atients and 101 control participants without leprosy.

21 teraction in the peripheral nerve lesions of leprosy.

22 contributes to nerve injury in patients with leprosy.

23 leprae, contributing to the pathogenesis of leprosy.

24 e expression profiles in the skin lesions of leprosy.

25 rium leprae is the noncultivable pathogen of leprosy.

26 identification of chains of transmission of leprosy.

27 in the lymphotoxin-alpha (LTalpha) gene and leprosy.

28 sceptibility to and clinical presentation of leprosy.

29 orm vs the self-limited, tuberculoid form of leprosy.

30 of chemotherapy on the overall incidence of leprosy.

31 nation of Mycobacterium leprae, the cause of leprosy.

32 and systemic complication of multibacillary leprosy.

33 l reactive antigen for specific diagnosis of leprosy.

34 he consequent reduction in the prevalence of leprosy.

35 this technique to track the transmission of leprosy.

36 morphism that is associated with lepromatous leprosy.

37 mune response contributes to nerve injury in leprosy.

38 nerve demyelination characteristic of human leprosy.

39 e drug discovery target for tuberculosis and leprosy.

40 ing to the control of host susceptibility to leprosy.

41 lopment of nerve injuries and deformities in leprosy.

42 mportance, such as plague, tuberculosis, and leprosy.

43 raphy in examination of peripheral nerves in leprosy.

44 rkinson's disease (PD), Crohn's disease, and leprosy.

45 in biopsy specimens from 85 individuals with leprosy.

46 lation are associated with increased risk of leprosy.

47 ns from patients with a disseminated form of leprosy.

48 identified gene conferring susceptibility to leprosy.

49 t a considerable proportion of patients with leprosy.

50 rae, the intracellular bacterium that causes leprosy.

51 detect latent tuberculosis in patients with leprosy.

52 xico, was diagnosed with diffuse lepromatous leprosy.

53 ved dapsone as part of multidrug therapy for leprosy (39 participants with the dapsone hypersensitivi

54 p of 5-7 years, out of 104 HHCs, 7 developed leprosy (6.7%).

55 ll-like receptors (TLRs) was investigated in leprosy, a spectral disease in which clinical manifestat

56 fic antibodies: the visual immunogold OnSite Leprosy Ab Rapid test [Gold-LFA] and the quantitative, l

57 LR expression at sites of disease such as in leprosy, acne, and psoriasis may be important in the pat

58 However, due to the spectral character of leprosy, additional, cellular biomarkers are required to

59 In a study of mainly paucibacillary leprosy-affected sib-pair families from South India, in

60 on WHO multidrug therapy for paucibacillary leprosy along with antiinflammatory drugs.

61 and Texas, there are autochthonous cases of leprosy among native-born Americans with no history of f

62 ssion in mycobacterial infection by studying leprosy, an intracellular infection caused by Mycobacter

63 were analyzed in 431 Ethiopian patients with leprosy and 187 control subjects.

64 Nerve damage is a clinical hallmark of leprosy and a major source of patient morbidity.

65 galectin-3 with unfavorable host response in leprosy and a potential mechanism for impaired host defe

66 pathogen associated with diffuse lepromatous leprosy and a reactional state known as Lucio's phenomen

67 besides diagnosing enlargement of nerves in leprosy and acute neuritis due to lepra reactions, guide

68 sed analysis revealed an association between leprosy and allele G of marker rs295340 (P = .042) and b

69 orderline evidence of an association between leprosy and alleles C and A of markers rs4880 (P = .077)

70 assist in the diagnosis and monitoring of MB leprosy and can detect a significant number of earlier-s

71 luding Parkinson's disease, Crohn's disease, leprosy and cancer.

72 atment of multiple myeloma, complications of leprosy and cancers.

73 tibility loci for chronic infections such as leprosy and chronic hepatitis B virus persistence.

74 for systemic juvenile idiopathic arthritis, leprosy and Crohn's disease.

75 sk variant function in rheumatoid arthritis, leprosy and Crohn's disease.

76 N-gamma responses only in the paucibacillary leprosy and household contact groups, with no responses

77 bility genes shared with Crohn's disease and leprosy and implicate mucosal factors and the innate imm

78 ), which occurs in patients with lepromatous leprosy and is characterized by neutrophil infiltration

79 Mycobacterium leprae causes leprosy and is unique among mycobacterial diseases in pr

80 teria, are associated with susceptibility to leprosy and its clinical outcomes.

81 immune response associated with lepromatous leprosy and may have important implications for understa

82 ed by the World Health Organization to treat leprosy and multi-drug-resistant tuberculosis.

83 y decrease an individual's susceptibility to leprosy and offer a novel therapeutic target for IL-1-de

84 tic intervention in modulating the course of leprosy and other chronic infectious diseases.

85 as a facile, genetically tractable model for leprosy and reveal the interplay between innate and adap

86 nd onchocerciasis), and infectious diseases (leprosy and South American (SA) blastomycosis), which ar

87 riants are associated with susceptibility to leprosy and the development of leprosy reactive states.

88 The slow onset of leprosy and the reliance on physical examination for det

89 cting findings about the association between leprosy and TLR1 variants N248S and I602S have been repo

90 ts to develop tools and approaches to detect leprosy and to stop the transmission of Mycobacterium le

91 Sera from leprosy and tuberculosis patients were also specific for

92 Leprosy and tuberculosis were widespread in the past and

93 protects against the mycobacterial diseases leprosy and tuberculosis.

94 rium, which includes the etiologic agents of leprosy and tuberculosis.

95 ics that are effective against tuberculosis, leprosy, and AIDS-related mycobacterial infections.

96 at possess activity against tuberculosis and leprosy, and an inhibitor of para-aminobenzoate biosynth

97 fection, periocular nerve involvement due to leprosy, and hypersensitivity reactions in tuberculosis.

98 s include HIV, herpes viruses, tuberculosis, leprosy, and malaria.

99 ase, resembles some aspects of tuberculosis, leprosy, and paratuberculosis.

100 mples from patients with multibacillary (MB) leprosy, and the rate of positive results declined with

101 ing the causative agents of tuberculosis and leprosy, are responsible for considerable morbidity and

102 Using leprosy as a model, we investigated whether expression o

103 ILRA2) regulates DC differentiation by using leprosy as a model.

104 atients with the different clinical types of leprosy as well as between the patients and 101 control

105 hogenesis, the management of nerve damage in leprosy, as in other demyelinating diseases, is extremel

106 including the inflammatory bowel disease and leprosy-associated tumor necrosis factor ligand superfam

107 s, despite their ancient separation, the two leprosy bacilli are remarkably conserved and still cause

108 suggest that the viability and purity of the leprosy bacilli used for in vitro studies determines the

109 when macrophages had a heavy burden of live leprosy bacilli.

110 Fortunately, the leprosy bacillus is sensitive to several antibiotics.

111 ly conserved in the degenerate genome of the leprosy bacillus, Mycobacterium leprae, indicating that

112 Here, we show that the leprosy bacterium hijacks this property to reprogram adu

113 A phylogeographic survey of 227 leprosy biopsies by differential PCR revealed that 221 c

114 ce of LTalpha on the control of experimental leprosy, both low- and high-dose Mycobacterium leprae fo

115 rial diseases explored include tuberculosis, leprosy, bubonic plague, typhoid, syphilis, endemic and

116 cells participate in the immune response in leprosy by their ability to activate T cells that recogn

117 In an analysis of a leprosy case-control study, iBVS selected 94 SNPs as pre

118 on to validate the findings of WES using 151 leprosy cases and 226 healthy controls by Sanger sequenc

119 pite the dramatic reduction in the number of leprosy cases worldwide in the 1990s, transmission of th

120 Leprosy, caused by infection with Mycobacterium leprae o

121 generative diseases including infection with leprosy-causing Mycobacterium leprae.

122 bacterium lepromatosis is a newly discovered leprosy-causing organism.

123 A key drug for the treatment of leprosy, clofazimine has recently been associated with h

124 We believe an all-out campaign by a global leprosy coalition is needed to bring that figure down to

125 nst lipid and peptide Ags of mycobacteria in leprosy, comparing tuberculoid patients, who are able to

126 48S is associated with an increased risk for leprosy, consistent with its hypoimmune regulatory funct

127 Leprosy control has seen little innovation and only limi

128 equired to block transmission and to improve leprosy control.

129 ons of patients with progressive lepromatous leprosy, correlating and colocalizing with IFN-beta and

130 Decubitus ulcer, psoriasis, and leprosy demonstrated review/protocol overrepresentation

131 e association study in Chinese patients with leprosy detected association signals in 16 single-nucleo

132 Since efficient leprosy diagnosis requires field-friendly test condition

133 With a prompt leprosy diagnosis, an early and effective treatment coul

134 th ESI-HRMS is a promising fast and sensible leprosy diagnostic method.

135 Mycobacterium leprae, the causative agent of leprosy, due to difficulties with culturing of the organ

136 will be a critical component of an effective leprosy elimination campaign.

137 Leprosy elimination has been a goal of the WHO for the p

138 ew strategies are required in the pursuit of leprosy elimination.

139 Leprosy enables investigation of mechanisms by which the

140 did not distinguish patients from EC in one leprosy-endemic area based on IFN-gamma.

141 He is a leading leprosy expert, ex-director of the world's premier agenc

142 Simple tests to facilitate referral to leprosy experts are not widely available, and the correc

143 and four healthy control relatives from two leprosy families.

144 , and CHGB48 and CHGB23 were susceptibile to leprosy for the male population, respectively).

145 e likely represents the first report of this leprosy form and its agent in the southeastern tip of Me

146 ere built from a cohort of 409 patients with leprosy from central Brazil, monitored for T1R and T2R.

147 e and adaptive immune determinants mediating leprosy granuloma formation and function.

148 The lepromatous leprosy granuloma is a dynamic entity requiring a steady

149 Understanding the pathogenesis of leprosy granulomas has been hindered by a paucity of tra

150 Mycobacterium leprae, which causes leprosy, grows optimally at approximately 30 degrees C,

151 Although the global prevalence of leprosy has decreased over the last few decades due to a

152 Leprosy has long been thought to have a strong genetic c

153 stigation into the innate immune response in leprosy has provided insight into immunoregulation in hu

154 T cells from patients with either cancer or leprosy has provided possible explanations for the alter

155 Since 2000, about 250 000 new cases of leprosy have been detected every year.

156 , the etiological agents of tuberculosis and leprosy, have coevolved with mammals for millions of yea

157 nd adaptive immunity, in the pathogenesis of leprosy, highlighting the merits of protein-coding varia

158 In the third cohort of schoolchildren from a leprosy hyperendemic region in Brazil, both tests detect

159 h T1R or T2R and controls with nonreactional leprosy identified the gene for interleukin 6 (IL-6) as

160 nal candidate gene SOD2 for association with leprosy in 2 independent population samples.

161 To address the persisting problem of leprosy in Cebu, Philippines, we compiled a database of

162 d feature elements resembling mid-borderline leprosy in humans.

163 ssary to investigate ongoing transmission of leprosy in regions of endemicity.

164 Red squirrels are thus a reservoir for leprosy in the British Isles.

165 dicated an association between TLR1 248S and leprosy in the case-control study (SS genotype odds rati

166 We performed a 3-stage GWAS of leprosy in the Chinese population using 8,313 cases and

167 Wild armadillos and many patients with leprosy in the southern United States are infected with

168 thogenic M. leprae, which is responsible for leprosy, in addition to its own parent cells.

169 e clinically progressive lepromatous form of leprosy; in contrast, galectin-3 was almost undetectable

170 obacterium leprae, the causative organism of leprosy, induced rapid demyelination by a contact-depend

171 the frequency of CD1b(+) DCs at the site of leprosy infection correlated with the clinical presentat

172 prae, the intracellular etiological agent of leprosy, infects Schwann promoting irreversible physical

173 nd with the potential for quality control in leprosy investigations.

174 Leprosy is a chronic but treatable infectious disease ca

175 Leprosy is a chronic disease characterized by skin and p

176 Leprosy is a chronic infectious disease caused by Mycoba

177 Diagnosis of leprosy is a major obstacle to disease control and has b

178 ts well-defined immunological complications, leprosy is a useful disease for studying genetic regulat

179 on from both tuberculosis and multibacillary leprosy is associated with heterozygosity for LTA4H poly

180 ently, the gold standard diagnostic test for leprosy is based on skin lesion biopsy, which is invasiv

181 Leprosy is caused by infection with Mycobacterium leprae

182 Leprosy is characterized by a spectrum of clinical manif

183 on of M. leprae in different countries where leprosy is endemic.

184 Early detection of leprosy is key to reduce the ongoing transmission.

185 razil, Ethiopia) and from South Korea, where leprosy is not endemic anymore.

186 Leprosy is not eradicable with currently available diagn

187 dely available, and the correct diagnosis of leprosy is often delayed.

188 Leprosy is present in more than 100 countries, where it

189 Leprosy is the most common form of treatable peripheral

190 ude the causative agents of tuberculosis and leprosy, is crucial for their success as pathogens.

191 Mycobacterium leprae, the causative agent of leprosy, is thought to be the mycobacterium most depende

192 cobacterium leprae, the organism that causes leprosy, is urgent in view of the continuing high levels

193 or the prevention of immune pathology during leprosy, it will not control bacterial burden and is the

194 s (also known as disseminated) form of human leprosy (L-lep), the origin and significance of these li

195 CD4(+) T cell clones derived from a leprosy lesion and patient blood were used to monitor th

196 LCs in leprosy lesions coexpress CD1a and langerin, placing LCs

197 vation correlated with mo-DC infiltration in leprosy lesions.

198 lgaris) have increasingly been observed with leprosy-like lesions on the head and limbs.

199 r, UK, showing skeletal signs of lepromatous leprosy (LL) have been studied using a multidisciplinary

200 a large natural reservoir for M. leprae, and leprosy may be a zoonosis in the region.

201 The chronic course of lepromatous leprosy may be interrupted by acute inflammatory episode

202 Leprosy morbidity is increased by 2 pathologic immune re

203 design of ErbB2 RTK-based therapies for both leprosy nerve damage and other demyelinating neurodegene

204 ls and mitochondrial swelling in pure neural leprosy nerves.

205 The impact of this regulation in leprosy neuropathy is discussed.

206 ypersensitivity syndrome among patients with leprosy (odds ratio, 6.18; P=3.84x10(-13)).

207 epidemiological surveys of the incidence of leprosy, of which little is known.

208 We found three new susceptible loci of leprosy, one in GAL3ST4 and two in CHGB.

209 h (trachoma and onchocerciasis), ulcer care (leprosy), or renal support (schistosomiasis).

210 not efficiently recognize lipid Ags from the leprosy pathogen, Mycobacterium leprae, or the related s

211 ae infection causes demyelination to mediate leprosy pathogenesis has been a long-standing question.

212 erium leprae to T cell clones derived from a leprosy patient in a CD1a-restricted and langerin-depend

213 re observed in the blood of a paucibacillary leprosy patient.

214 kin tests from the same individual, from 113 leprosy patients and 104 household contacts of patients

215 variants in Han Chinese, of whom were 7,048 leprosy patients and 14,398 were healthy control subject

216 tested for IFN-gamma responses in PBMC from leprosy patients and contacts, tuberculosis patients, an

217 es induced by M. leprae proteins in blood of leprosy patients and endemic controls (EC) from high lep

218 In this study, we used WES approach on four leprosy patients and four healthy control relatives from

219 sponses from both TB and paucibacillary (PB) leprosy patients and from healthy household contacts of

220 ollection of M. leprae isolates derived from leprosy patients and propagated in armadillo hosts.

221 The immune response of leprosy patients can be highly diverse, ranging from str

222 f this work was to identify lipid markers in leprosy patients directly from skin imprints, using a ma

223 d directly to archived tissue specimens from leprosy patients for the purpose of molecular typing by

224 peptides that provide specific responses in leprosy patients from an endemic setting could potential

225 sting was performed on skin biopsies from 24 leprosy patients from Guinea-Conakry for the first time.

226 clones derived from the cutaneous lesions of leprosy patients have been shown to recognize specifical

227 luation of sera from 20 clinically diagnosed leprosy patients using native protein and recombinant pr

228 Schwann cells in skin lesions from leprosy patients were found to express TLR2.

229 Forty multibacillary leprosy patients were negative.

230 Five of 10 paucibacillary leprosy patients were Quantiferon Gold (Q-G) positive wi

231 roarrays were applied to investigate whether leprosy patients with different clinical forms of the di

232 Pentraxin-3 (PTX3) analyses of sera from 87 leprosy patients with or without reactions were conducte

233 y and apoptotic molecules were identified as leprosy patients' markers.

234 on incubation with blood from paucibacillary leprosy patients, a group who limit M. leprae growth and

235 d in lesions and after TLR activation in all leprosy patients, CD1b+ dendritic cells were not detecte

236 clinical diagnosis, thus demonstrating that leprosy patients, including those diagnosed with the pau

237 a major cause of peripheral nerve damage in leprosy patients, the immunopathogenesis of ENL remains

238 cterium leprae-reactive T cells derived from leprosy patients, while cytokine profiles of LILRA2-acti

239 esults of a genome-wide association study of leprosy per se, we investigated the TNFSF15 chromosomal

240 Leprosy persists as a public health problem.

241 h antileprosy drug resistance occurs in this leprosy population, resistance does not appear to be a m

242 Leprosy presents as a clinical and immunological spectru

243 Leprosy presents with a clinical spectrum of skin lesion

244 therapy have dramatically reduced worldwide leprosy prevalence, but new case detection rates have re

245 ffered between EC from areas with dissimilar leprosy prevalence.

246 patients and endemic controls (EC) from high leprosy-prevalence areas (Bangladesh, Brazil, Ethiopia)

247 erence Laboratory (NTRL) and National TB and Leprosy Program redesigned the tuberculosis specimen tra

248 screening of contacts of known patients with leprosy promises to strengthen early diagnosis, while pr

249 Leprosy provides a model to investigate mechanisms of im

250 Identifying genetic predictive factors for leprosy reactions may have a major impact on preventive

251 eptibility to leprosy and the development of leprosy reactive states.

252 associated with increased susceptibility to leprosy (recessive, P = 1.4 x 10(-3)) and with increased

253 Leprosy remains a major global health problem and typica

254 Leprosy remains an important health problem in a number

255 infection should therefore be emphasized in leprosy research.

256 Study of IFN responses in human leprosy revealed an inverse correlation between IFN-beta

257 wild armadillo and three U.S. patients with leprosy revealed that the infective strains were essenti

258 nificant role for TLR-2 in the occurrence of leprosy reversal reaction and provide new insights into

259 7 of 28 SA blastomycosis (25%), and 14 of 83 leprosy sera (17%).

260 report, we evaluate the performance of a new leprosy serological test (NDO-LID).

261 ecommended that all registered patients with leprosy should receive combination therapy with three an

262 osy susceptibility factors in 474 Vietnamese leprosy simplex families.

263 ies of gene expression profiles derived from leprosy skin lesions suggested a link between IL-27 and

264 Development of a leprosy-specific vaccine that boosts long-lasting T-cell

265 dge potential for diagnosis across the whole leprosy spectrum.

266 is associated with a decreased incidence of leprosy, suggesting that Mycobacterium leprae subverts t

267 Here, we studied these 16 SNPs as potential leprosy susceptibility factors in 474 Vietnamese leprosy

268 HLA-DR-DQ, RIPK2, CCDC122-LACC1, and NOD2 as leprosy susceptibility factors in Vietnam.

269 pic effects demonstrated a high tendency for leprosy susceptibility loci to show association with aut

270 The MICA*5A5.1 allele, associated here with leprosy susceptibility, encodes a protein lacking a cyto

271 contribution of common noncoding variants to leprosy susceptibility, protein-coding variants have not

272 The striking finding was that in lepromatous leprosy, T cells did not efficiently recognize lipid Ags

273 Leprosy takes many years to manifest, and this has precl

274 an the alternative, the Standard Diagnostics leprosy test (87.0% versus 81.7% and 32.3% versus 6.5%,

275 er proportions of MB and paucibacillary (PB) leprosy than the alternative, the Standard Diagnostics l

276 dicating a role in genetic susceptibility to leprosy that is independent of HLA-DRB1.

277 Mycobacterium leprae, a well-known cause of leprosy, that justifies the status of M. lepromatosis as

278 ns to tuberculosis and reversal reactions in leprosy, the exact mechanisms, and therefore potential d

279 Leprosy, the leading infectious cause of disability worl

280 of thioamide drugs to treat tuberculosis and leprosy, their precise mechanisms of action remain unkno

281 To develop an animal model for leprosy, three black mangabeys (BkMs) (Lophocebus aterri

282 ment could be feasible and thus the chain of leprosy transmission could be abbreviated.

283 or targeted approaches to search and confirm leprosy transmission in various scenarios.

284 The first antibiotic to be widely used for leprosy treatment was dapsone in the 1950s, which had to

285 ion and the identification or testing of new leprosy treatments.

286 In leprosy, type 1 reaction (T1R) and type 2 reaction (T2R)

287 We report a case of leprosy unmasking and downgrading reaction after stem ce

288 Research on tuberculosis and leprosy was revolutionized by the development of a plasm

289 ne development of the immune response during leprosy we have developed an M. leprae ear infection mod

290 In the human mycobacterial infection leprosy, we found that activation of monocytes via nucle

291 obacterium leprae, the causative organism of leprosy, we identified that intracellular M. leprae acti

292 hisms were associated with susceptibility to leprosy when comparing allele frequencies, and 8 were as

293 used to study the genetic susceptibility to leprosy,while whole exome sequencing (WES) approach has

294 discovery of several susceptibility loci for leprosy with robust evidence, providing biological insig

295 estations seen in patients, from tuberculoid leprosy with robust production of Th1-type cytokines to

296 ted by comparing results in HHCs who develop leprosy with those not affected.

297 y was consistent with borderline tuberculoid leprosy with type 1 lepra reaction.

298 cally expressed in the polar immune forms of leprosy, with type I IFNs inducing IL-10 that interferes

299 lary disease is similar to human lepromatous leprosy, with variable/high levels of antibody and a dys

300 been implicated in the pathogenesis of human leprosy, yet it is not clear whether Mycobacterium lepra