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1 risk for CL development caused by Leishmania braziliensis.
2 d an effective treatment for CL caused by L. braziliensis.
3 reatment of tegumentary disease caused by L. braziliensis.
4 eous leishmaniasis (CL) caused by Leishmania braziliensis.
5 bundant in skin lesions caused by Leishmania braziliensis.
6 cutaneous leishmaniasis caused by Leishmania braziliensis.
7 brucei and to a lesser extent in Leishmania braziliensis.
8 the clinical course of diseases caused by L. braziliensis.
9 ed with the prevalent related species L.(V.) braziliensis.
10 we characterized DCs that were exposed to L. braziliensis.
11 ishmania: Leishmania infantum and Leishmania braziliensis.
12 to LCTAS, were isolated and mapped onto a L. braziliensis 250 kb multicopy minichromosome and the L.
14 Here we show that ROS inhibits growth of L. braziliensis amastigotes in resting monocytes, and that
15 Monocytes from PBMC were infected with L. braziliensis and cocultured with CD8(+) T cells, and the
18 S in the telomeric region differs between L. braziliensis and L. major: in L. major the LCTASs are ta
20 ll RNAs derived from LRV1 in both Leishmania braziliensis and Leishmania guyanensis, mapping across b
21 results against Trypnosoma cruzi, Leishmania braziliensis and Leishmania infantum were not clinically
22 300 telomere-derived clones from Leishmania braziliensis and Leishmania major, a conserved 100 bp se
24 nuclear cells from patients infected with L. braziliensis and reduced IL-1beta levels after cure.
25 cessfully generated axenic amastigotes of L. braziliensis and used them to test the hypothesis that L
26 second Brazilian sample (also exposed to L. braziliensis) and in Iranians infected with Leishmania t
27 Lutzomyia intermedia, a vector of Leishmania braziliensis, and evaluated the seroreactivity in expose
28 hmania (Leishmania) amazonensis, L (Viannia) braziliensis, and L (V) guyanensis] and samples from pat
29 were established, parasites were typed as L. braziliensis, and the presence of LRV1 was determined by
30 th cutaneous leishmaniasis due to Leishmania braziliensis are CD4(+)CD25(-)CD127(-/low)FOXP3(-) cells
34 are of patients with CL caused by Leishmania braziliensis, because screening for and treatment of hel
35 ows that ROS are important for control of L. braziliensis both at the initial stages of infection, as
45 ed Leishmania proteins, Leishmania (Viannia) braziliensis-derived Lb8E and Lb6H, and evaluated both i
46 that human patients infected with Leishmania braziliensis develop dysbiotic skin microbiota, characte
49 eous leishmaniasis (CL) caused by Leishmania braziliensis in Brazil with pentavalent antimony (Sb(v))
51 eous leishmaniasis patients infected with L. braziliensis in Rio de Janeiro, Brazil, an area where th
53 The chemoattractant factors secreted by L. braziliensis-infected cells were highly efficient in rec
54 wide transcriptional profiling of Leishmania braziliensis-infected cutaneous lesions and normal skin
56 ood mononuclear cells (PBMC) from Leishmania braziliensis-infected human patients have demonstrated t
57 cytokines and prime naive CD4(+) T cells, L. braziliensis-infected MyD88(-/-) DCs exhibited less acti
58 drug treatment success and disease in 97 L. braziliensis-infected patients from Peru and Bolivia.
60 We have previously reported that Leishmania braziliensis infection can activate murine dendritic cel
61 of inflammatory mediators in response to L. braziliensis infection contributes to cell recruitment a
62 and used them to test the hypothesis that L. braziliensis infection efficiently triggers innate respo
64 Cutaneous leishmaniasis due to Leishmania braziliensis infection is an inflammatory disease in whi
73 e findings uncover a dual role for DCs in L. braziliensis infection: T cell activation by bystander D
75 eous leishmaniasis (CL) caused by Leishmania braziliensis is associated with high levels of tumor nec
76 eous leishmaniasis (CL) caused by Leishmania braziliensis is characterized by a strong Th1 response t
80 iasis, caused in South America by Leishmania braziliensis, is difficult to cure by chemotherapy (prim
81 d SC expression associated with 2 primary L. braziliensis isolates from patients with LCL or MCL.
82 east 70-77% of their sterol from leucine; L. braziliensis, L. donovani and L. tropica apparently prod
83 riTrypDB integrates datasets from Leishmania braziliensis, L. infantum, L. major, L. tarentolae, Tryp
84 tro against Leishmania infantum , Leishmania braziliensis , Leishmania guyanensis , Leishmania amazon
85 omplexes of New World Leishmania (Leishmania braziliensis, Leishmania mexicana, and Leishmania donova
86 suggest that if local therapy for single L. braziliensis lesions is chosen, this treatment is attrac
97 braziliensis, LRV-1-positive strains of L.V. braziliensis produced a predominant Th2-biased immune re
100 s the human immune response, facilitating L. braziliensis survival in vitro, and increases the risk o
102 oss-protected mice against infection with L. braziliensis that causes mucocutaneous leishmaniasis.
103 he LCTASs are tandemly repeated, while in L. braziliensis the LCTAS is present as a single copy per e
104 .6%) did not have evidence of exposure to L. braziliensis The ratio of infection to disease was 3.2:1
105 in vitro a role for LRV1 in virulence of L. braziliensis, the Leishmania species responsible for the
106 the generation of protective immunity to L. braziliensis, TLR2 seems to have a regulatory role durin
108 en 1992 and 1998 in an area where Leishmania braziliensis transmission is endemic; 8 of the patients
109 w that IL-1beta production in response to L. braziliensis was dependent on NLRP3, caspase-1, and casp
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