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1                                              L. amazonensis amastigotes, through activation of extrac
2                                              L. amazonensis is endemic in South America, where it cau
3                                              L. amazonensis metacyclic promastigotes lacking one SODA
4    Inhibition of arginase I or ODC abrogates L. amazonensis replication in infected human macrophages
5                                 In addition, L. amazonensis infection induces an early increase in To
6 ole in downmodulating the Th1 response after L. amazonensis infection.
7 htly more potent than amphotericin B against L. amazonensis.
8 sm underlying this enhanced immunity against L. amazonensis infection remains largely unresolved.
9 f a DNA vaccine to induce protection against L. amazonensis infection.
10 ed in the protective immune response against L. amazonensis infection in vaccinated mice.
11  compound 4 exhibited better results against L. amazonensis promastigotes (IC(50) = 15.52 3.782 uM) a
12                                     Although L. amazonensis lacking LIT1 grew normally in axenic cult
13 s encoding murine interleukin-12 (IL-12) and L. amazonensis HSP70.
14 d and tested against Leishmania donovani and L. amazonensis intracellular amastigotes.
15 ation of virulent forms in both L. major and L. amazonensis Our results also uncover a unique require
16 s that cause cutaneous disease, L. major and L. amazonensis, are poorly understood.
17 ALB/c mice to infection with L. mexicana and L. amazonensis, does play a significant role in regulati
18 ed by the New World species, L. mexicana and L. amazonensis, we analyzed their course of infection in
19 plex parasites (L. mexicana, L. pifanoi, and L. amazonensis), a critical role for immunoglobulin G-me
20 inst Leishmania spp promastigotes as well as L. amazonensis and L. infantum amastigotes.
21  subset of phagocytic B (termed B-1P) cells, L. amazonensis survives and proliferates at high rates i
22 that the CD4+ T-cell response during chronic L. amazonensis infection is limited during the transitio
23 c Th1 transfer helped recipient mice control L. amazonensis infection established by promastigotes bu
24 particular, neutrophil-derived LTB4 controls L. amazonensis killing, degranulation, and reactive oxyg
25          In comparison to L. major controls, L. amazonensis-infected DCs secreted lower levels of int
26    All phenotypes observed in LHR1/Deltalhr1 L. amazonensis were rescued by expression of episomal LH
27 r inhibiting PERK kinase activity diminished L. amazonensis infection.
28 of the Dectin-1/Syk/ROS/NLRP3 pathway during L. amazonensis phagocytosis is important for macrophage
29     We identified that ROS production during L. amazonensis infection occurs upon engagement of Decti
30  in regulating local immune responses during L. amazonensis infection, providing new insights into im
31 ression in C57BL/6 mice infected with either L. amazonensis or L. major (a healing model).
32 crophages from 5-LO knockout mice eliminated L. amazonensis in the presence of exogenous LTB4, and ma
33  from P2X7 receptor knockout mice eliminated L. amazonensis when incubated with ionomycin.
34 acts (SGE) of Lutzomyia longipalpis enhances L. amazonensis infection.
35 es revealed that Retro-2 curbed experimental L. amazonensis infections in a dose-dependent manner.
36 e were injected locally with IP-10 following L. amazonensis infection, there was a significant delay
37 ls, as local injection of IL-1beta following L. amazonensis infection accelerated Th cell activation
38 n and interleukin-12p40 production following L. amazonensis amastigote infection compared with non-tr
39 ion represents a required upstream event for L. amazonensis-induced LTB4 synthesis.
40 ads to LTB4 formation, which is required for L. amazonensis elimination.
41  the importance of efficient heme uptake for L. amazonensis replication and vertebrate host infectivi
42 comparison of draining lymph node cells from L. amazonensis- and L. major-infected mice at 10 weeks p
43     Antigen stimulation of CD4+ T cells from L. amazonensis-infected mice in vitro in the presence of
44  (IFN-gamma) production of CD4+ T cells from L. amazonensis-infected mice.
45           However, these cells isolated from L. amazonensis-infected mice were not skewed toward eith
46 hmania amazonensis Our inability to generate L. amazonensis SODA null mutants and the lethal phenotyp
47 functional B cells are important for healing L. amazonensis in this infectious disease model.
48 nal antibodies (MoAbs) against a non-healing L. amazonensis infection in BALB/c mice, and that anti-P
49                                           In L. amazonensis, reactive oxygen species (ROS) signaling
50 emonstrated after expression in yeast and in L. amazonensis LIT1-null amastigotes.
51        The disease-promoting CD4+ T cells in L. amazonensis-infected mice have the characteristics of
52  was reported for L. major, APX depletion in L. amazonensis enhanced differentiation of metacyclic pr
53 ization and membrane association of FCaBP in L. amazonensis suggest that the mechanisms for flagellar
54 ributed partially to compromised immunity in L. amazonensis-infected hosts.
55 hondrial alterations and lipid inclusions in L. amazonensis promastigotes, upregulated tumor necrosis
56 responses contributes to the pathogenesis in L. amazonensis-infected mice.
57 responsible for the susceptible phenotype in L. amazonensis-infected hosts and that this parasite may
58 production, may limit the immune response in L. amazonensis-infected mice.
59                In contrast, we found that in L. amazonensis, the ROS-inducible APX is essential for s
60 ver, the adoptive transfer of ANK cells into L. amazonensis-infected mice markedly increased DC and T
61 ole in its activity against intramacrophagic L. amazonensis.
62 ng an important effector function in killing L. amazonensis.
63 LHR1-complemented (LHR1/Deltalhr1 plus LHR1) L. amazonensis strains.
64                             L. major (LV39), L. amazonensis and L. mexicana were the most efficient u
65     In phagocytic cells such as macrophages, L. amazonensis modulates endosomal/lysosomal trafficking
66 head challenge infection with 107 metacyclic L. amazonensis promastigotes at 4 wk demonstrated protec
67 d amastigotes in IFN-gamma-stimulated Mphis, L. amazonensis-specific Th1 transfer helped recipient mi
68 fection established by promastigotes but not L. amazonensis infection established by amastigotes.
69                                     Notably, L. amazonensis amastigote infection failed to activate D
70 , we identify and characterize LIT1, a novel L. amazonensis membrane protein with extensive similarit
71 f interleukin-10 (IL-10), in CD4(+) cells of L. amazonensis-infected mice, we further examined whethe
72                               The failure of L. amazonensis-infected C3H mice to respond to IL-12 was
73  PD-1 and PD-L1 in the immunopathogenesis of L. amazonensis infection in C57BL/6 mice.
74 lation of the macrophage-mediated killing of L. amazonensis in vitro and a less robust antibody respo
75 e ear with 10(5) metacyclic promastigotes of L. amazonensis together with SGE (equivalent to 0.5 glan
76  and successful intracellular replication of L. amazonensis.
77 he complicated pathogenic immune response of L. amazonensis.
78 via NADPH oxidase during the early stages of L. amazonensis infection is critical for inflammasome ac
79 ranscription-PCR in all life-cycle stages of L. amazonensis.
80                         Adoptive transfer of L. amazonensis-specific Th1 cells prior to infection ove
81                                 Treatment of L. amazonensis-infected mice with the highly-specific mi
82 ent mice infected with either L. mexicana or L. amazonensis failed to control the lesion progression,
83 rprised to find that IFN-gamma could promote L. amazonensis amastigote replication in macrophages (Mp
84  we observed that ATP was not able to reduce L. amazonensis load.
85          This was supported by the fact that L. amazonensis amastigotes limited the production of IL-
86             These experiments indicated that L. amazonensis resistance to killing in vivo is only par
87 iginal sites of inoculation, indicating that L. amazonensis can persist in vivo independently of the
88              In this study, we observed that L. amazonensis induced PD-1 expression on both CD4(+) an
89                  In this study, we show that L. amazonensis or its lipophosphoglycan can induce neutr
90                 Previous studies showed that L. amazonensis incorporates heme through the transmembra
91                We have previously shown that L. amazonensis-infected C57BL/6 mice have profound impai
92                   These results suggest that L. amazonensis amastigotes may condition DCs of a suscep
93 ults reveal a quite unexpected aspect of the L. amazonensis parasite and have important implications
94 ential of a DNA-based vaccine, we tested the L. amazonensis gene encoding P4 nuclease as well as adju
95                  One possibility is that the L. amazonensis parasite modulates antigen-presenting cel
96         Moreover, we immunized mice with the L. amazonensis vaccines to determine if this vaccine reg
97 ay not always be indicative of protection to L. amazonensis infection.
98 tion in macrophages, and mouse resistance to L. amazonensis infection in vivo.
99 ngly, inflammasome activation in response to L. amazonensis is impaired by inhibitors of NADPH oxidas
100  pathology, and therefore, susceptibility to L. amazonensis infection.
101 because IL-4-/- mice remained susceptible to L. amazonensis infection, even after IL-12 administratio
102                          After 2 to 4 weeks, L. amazonensis-infected mice had significantly delayed a
103 se mechanism of pathogenesis associated with L. amazonensis infection remains largely unresolved.
104  of bone marrow-derived dendritic cells with L. amazonensis amastigotes resulted in rapid and signifi
105 4/IL-12, or P4/HSP70 prior to challenge with L. amazonensis promastigotes.
106  protective response in mice challenged with L. amazonensis and L. pifanoi.
107  infection of C3HeB/FeJ mice for 7 days with L. amazonensis promoted an immature CD11c(+) DC phenotyp
108  between MHC class II -/- mice infected with L. amazonensis and Leishmania major suggest that these p
109 e response of mice chronically infected with L. amazonensis can be enhanced towards a Th1 phenotype b
110         We found that C3H mice infected with L. amazonensis exhibited decreased IL-12 production, whi
111  functions at early stages of infection with L. amazonensis parasites and provide a compelling ration
112                               Infection with L. amazonensis promastigotes led to increased 1/2 phosph
113 cells exposed to SGE prior to infection with L. amazonensis.
114 d dendritic cells (DCs) of C57BL/6 mice with L. amazonensis or Leishmania major promastigotes and ass
115  could be enhanced in vitro and in vivo with L. amazonensis antigen-pulsed bone marrow-derived dendri
116                                          Yet L. amazonensis-infected DCs produced elevated levels of

 
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