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1 cellular parasites Rickettsia prowazekii and Mycobacterium leprae.
2 aired mitogenesis in response to antigens of Mycobacterium leprae.
3 logy with Mn-superoxide dismutase of MAC and Mycobacterium leprae.
4 tro, monocytes produced IL-18 in response to Mycobacterium leprae.
5 associated with active cellular immunity to Mycobacterium leprae.
6 man pathogens Mycobacterium tuberculosis and Mycobacterium leprae.
7 atients, who have potent T cell responses to Mycobacterium leprae.
8 e-rich antigens found in M. tuberculosis and Mycobacterium leprae.
9 libraries of Mycobacterium tuberculosis and Mycobacterium leprae.
10 ), parvovirus B19, variola virus (VARV), and Mycobacterium leprae.
11 gy and immune responses that fail to control Mycobacterium leprae.
12 to be Mycobacterium lepromatosis instead of Mycobacterium leprae.
13 cells by an intracellular bacterial pathogen Mycobacterium leprae.
14 predicted for Mycobacterium tuberculosis and Mycobacterium leprae.
15 ux pump in all sequenced mycobacteria except Mycobacterium leprae.
16 eprosy, an intracellular infection caused by Mycobacterium leprae.
17 rol to reduce cases and curb transmission of Mycobacterium leprae.
18 in Mexico, wild armadillos are infected with Mycobacterium leprae.
19 disease caused by the intracellular pathogen Mycobacterium leprae.
20 Leprosy is caused by infection with Mycobacterium leprae.
21 ses including infection with leprosy-causing Mycobacterium leprae.
22 proteins are conserved within the genome of Mycobacterium leprae.
23 h the type of immune response mounted toward Mycobacterium leprae.
24 Humans are considered as the main host for Mycobacterium leprae(1), the aetiological agent of lepro
26 ising the N-terminal portion of the putative Mycobacterium leprae 19-kDa lipoprotein, triggered an in
29 egments revealed significant divergence from Mycobacterium leprae, a well-known cause of leprosy, tha
30 possible to distinguish different strains of Mycobacterium leprae according to their genetic sequence
33 /nu) mice were infected in the footpads with Mycobacterium leprae and fed a linoleic acid-free diet.
34 ns is largely determined by host immunity to Mycobacterium leprae and is a model for immunoregulation
36 rallel host immunity to its causative agents Mycobacterium leprae and Mycobacterium lepromatosis.
37 Comparison of ancient and modern genomes of Mycobacterium leprae and Mycobacterium tuberculosis give
38 overall) and is 50% identical to FAP of both Mycobacterium leprae and Mycobacterium tuberculosis.
41 een shown to recognize specifically LAM from Mycobacterium leprae and not from M. tuberculosis Erdman
42 lar bacterial pathogens in humans, including Mycobacterium leprae and Salmonella enterica serovar Typ
43 lysis to identify genes that are specific to Mycobacterium leprae and tested both recombinant protein
44 gated the role of TLRs in the recognition of Mycobacterium leprae and the significance of TLR2Arg(677
46 tions in codon 53 or 55 of the folP1 gene of Mycobacterium leprae, and definitive evidence linking th
48 Several Mycobacterium tuberculosis strains, Mycobacterium leprae, and other mycobacterial pathogens
49 ll wall layer of Mycobacterium tuberculosis, Mycobacterium leprae, and several opportunistic mycobact
50 s infectious disease caused by the pathogen, Mycobacterium leprae, and the more recently discovered,
54 resistance surveillance and strain typing of Mycobacterium leprae are necessary to investigate ongoin
55 s secreted 3 hours after treating PBMCs with Mycobacterium leprae as compared with 48 hours for IFN-g
57 obalance sensor was developed for sensing of Mycobacterium leprae bacteria through its epitope sequen
58 plied to the obligate intracellular organism Mycobacterium leprae because of the difficulty of obtain
59 or/interleukin-10 ratio when stimulated with Mycobacterium leprae but not with lipopolysaccharide or
60 ctional homology of the Nramp homologue from Mycobacterium leprae by using a yeast complementation as
64 prosy, which is caused by the human pathogen Mycobacterium leprae, causes nerve damage, deformity and
65 rkers to induce cellular immune responses to Mycobacterium leprae: CD1a mediates the presentation of
66 lenge in animal models, for efficacy against Mycobacterium leprae challenge in a murine model of lepr
69 ng pathogen-associated molecular patterns of Mycobacterium leprae, cytokine release by innate immune
70 sis and then therapeutically vaccinated with Mycobacterium leprae-derived hsp65 DNA develop severe gr
72 xperimental leprosy, both low- and high-dose Mycobacterium leprae foot pad (FP) infections were evalu
73 ple sequence repeats, or microsatellites, in Mycobacterium leprae from patients living in and around
74 NA sequence analysis of cosmid L373 from the Mycobacterium leprae genome, an open reading frame of 1.
75 odel for the accretion of pseudogenes in the Mycobacterium leprae genome, triggered by the loss of di
76 n in animals and cultures, the cell walls of Mycobacterium leprae grown in armadillos was characteriz
77 A DNA vaccine encoding the hsp60 molecule of Mycobacterium leprae has previously been shown to protec
79 NA) approaches on the major causative agent, Mycobacterium leprae, have elucidated the disease's evol
80 ifloxacin, and assessed the potential of the Mycobacterium leprae heat shock protein-65 DNA vaccine t
85 loped an in vitro model to study the fate of Mycobacterium leprae in a LL lesion, with and without im
86 es, including Mycobacterium tuberculosis and Mycobacterium leprae in addition to Mab, supporting the
88 gle nucleotide polymorphism (SNP) typing for Mycobacterium leprae in biopsied skin lesion samples.
89 unit of the phenolic glycolipid-1 (PGL-1) of Mycobacterium leprae in determining the bacterial predil
90 m baseline in the odds of positive growth of Mycobacterium leprae in mouse footpads after 8 weeks of
91 f IL-12Rbeta2 on T cells was up-regulated by Mycobacterium leprae in tuberculoid but not in lepromato
93 ctivate T cells that recognize the pathogen, Mycobacterium leprae, in a langerin-dependent manner.
94 , with the exception of the peptidoglycan of Mycobacterium leprae, in which glycine replaces the L-al
96 e degenerate genome of the leprosy bacillus, Mycobacterium leprae, indicating that non-essential func
99 Herein, a global gene expression profile of Mycobacterium leprae-infected primary human Schwann cell
105 the molecular basis of the neural tropism of Mycobacterium leprae is attributable to the specific bin
106 To understand how the immune response to Mycobacterium leprae is regulated, human dendritic cells
110 rosy, a chronic infectious disease caused by Mycobacterium leprae, is prevalent in India, where about
111 1990s, transmission of the causative agent, Mycobacterium leprae, is still occurring, and new cases
113 - Mycobacterium tuberculosis (tuberculosis), Mycobacterium leprae (leprosy) and Treponema pallidum pa
115 atis and like Mycobacterium tuberculosis and Mycobacterium leprae, M. marinum was shown to possess a
116 d two other crystal structures for RuvA from Mycobacterium leprae (MleRuvA) and EcoRuvA showed that i
117 smegmatis with the homologous sequences from Mycobacterium leprae, Mycobacterium bovis, and Mycobacte
118 of leprosy, attributed to early invasion by Mycobacterium leprae of Schwann cells related to unmyeli
119 glected chronic infectious disease caused by Mycobacterium leprae or M. lepromatosis, representing a
120 wing exposure to Mycobacterium tuberculosis, Mycobacterium leprae or Mycobacterium avium is correlate
122 cognize lipid Ags from the leprosy pathogen, Mycobacterium leprae, or the related species, Mycobacter
123 terium tuberculosis, Mycobacterium bovis, or Mycobacterium leprae; or in the non-mycobacterial Actino
124 Accordingly, comparative bioinformatics and Mycobacterium leprae protein microarrays were applied to
125 d demyelination and axonal injury induced by Mycobacterium leprae provides a model for elucidating th
126 n to both CD1b- and MHC class II-restricted, Mycobacterium leprae-reactive T cells derived from lepro
129 riation by neutron scattering was applied to Mycobacterium leprae RuvA (MleRuvA), a synthetic analogu
131 ilarity to the enzyme from cyanobacteria and Mycobacterium leprae, similarity to the conserved transa
132 d lateral flow assays (LFA) for detection of Mycobacterium leprae-specific antibodies: the visual imm
136 treatment with five different microbial hsp (Mycobacterium leprae, Streptococcus pneumoniae, Helicoba
137 reased incidence of leprosy, suggesting that Mycobacterium leprae subverts the TLR system as a mechan
138 conserved in Mycobacterium tuberculosis and Mycobacterium leprae, suggesting that regulation of DNA
140 to investigate the molecular epidemiology of Mycobacterium leprae, the causative agent of leprosy, du
143 tect leprosy and to stop the transmission of Mycobacterium leprae, the causative bacillus of the dise
146 wann cell response to long-term infection of Mycobacterium leprae, the causative organism of leprosy,
147 hown to serve as a Schwann cell receptor for Mycobacterium leprae, the causative organism of leprosy.
150 ing treatment of monocytes with IFN-beta and Mycobacterium leprae, the intracellular bacterium that c
152 tools for the differentiation of isolates of Mycobacterium leprae, the organism that causes leprosy,
153 ng characteristics of the causative bacillus Mycobacterium leprae: the long incubation period, limite
154 xide stress response in enteric bacteria) in Mycobacterium leprae, this gene is inactive in all strai
155 six new proteins isolated from in vivo-grown Mycobacterium leprae, three of which correspond to produ
156 idermal LCs presented nonpeptide antigens of Mycobacterium leprae to T cell clones derived from a lep
157 the species-specific phenolic glycolipid of Mycobacterium leprae triggers uptake into Schwann cells
159 idoglycan from in vivo-derived noncultivable Mycobacterium leprae was assumed to possess the basic st
160 otide sequence of 1.5 Mb of genomic DNA from Mycobacterium leprae was determined using computer-assis
162 PBMC of tuberculoid patients stimulated with Mycobacterium leprae was partially inhibited by mAbs to
165 ganization of TrxR and Trx has been found in Mycobacterium leprae, where TrxR and Trx are encoded by
166 prosy phenotypes as well as high exposure to Mycobacterium leprae which respectively allow improved d
168 f human leprosy, yet it is not clear whether Mycobacterium leprae, which has a distinct MDP structure
169 exican patient, and compared it with that of Mycobacterium leprae, which has undergone extensive redu
170 sy is a chronic infectious disease caused by Mycobacterium leprae, which primarily infects macrophage
171 me sequences of certain pathogenic bacteria (Mycobacterium leprae, Yersinia pestis and Rickettsia pro