ライフサイエンスコーパス: T. cruzi

1 T. cruzi autophagin-2 (TcAtg4.2) carries the majority of

2 T. cruzi calreticulin (TcCalr) is a multifunctional, end

3 T. cruzi immune serum prevented CD8(+) T cell functional

4 T. cruzi induced differential polarization of immunoregu

5 T. cruzi infection also seems to confer protection again

6 T. cruzi infection can be acquired at or near the bite s

7 T. cruzi infection enhanced tissue expression of MBL bot

8 T. cruzi infection, in vitro, was able to stimulate the

9 T. cruzi strains resistant to BZ were also found to be r

10 T. cruzi-immune CCR5(-/-) and wild-type C57BL/6 mice wer

11 T. cruzi-specific IgG was detected in sera from infected

12 Prospective study involving 144 T. cruzi seropositive pregnant women.

13 F-beta1, IDO, and programmed death ligand 2, T. cruzi infection induced an early increase of Gal-1 ex

14 A T. cruzi strain overexpressing the Poltheta-helicase dom

15 We established a T. cruzi strain expressing green fluorescent protein (GF

16 efficacy of selected hits were assessed in a T. cruzi mouse model, where 6a and 6b reduced parasitemi

17 to potent analogues with low nM IC(50)s in a T. cruzi whole cell in vitro assay.

18 processes taking place the hearts of acutely T. cruzi-infected mice.

19 f activity of human defensin alpha-1 against T. cruzi and its function may provide insights for the d

20 to TcCYP51 and significant activity against T. cruzi amastigotes cultured in human myoblasts (EC50 =

21 times more potent than benznidazole against T. cruzi and slightly more potent than amphotericin B ag

22 s of cross-screening these compounds against T. cruzi, L. donovani, and S. mansoni.

23 pic screen of a library of compounds against T. cruzi.

24 crucial step for vaccine development against T. cruzi.

25 r a new mechanism in innate immunity against T. cruzi infection mediated by Trk signaling akin to an

26 t required for early host protection against T. cruzi.

27 ase, not only in the immune response against T. cruzi, but also in mediating cardiac tissue damage.

28 nergic activity between two terpenes against T. cruzi.

29 osaconazole, a drug proposed for use against T. cruzi infections, in combination with benznidazole.

30 tes for the development of a vaccine against T. cruzi.

31 es 2 and 4 were more active in vitro against T. cruzi and less toxic against Vero cells than both the

32 resulting from cardiac dysfunction, although T. cruzi infection results in inflammation and cell dest

33 arasitic trypanosomes Trypanosoma brucei and T. cruzi are responsible for significant human suffering

34 cant activity against Trypanosoma brucei and T. cruzi, featuring favorable drug-like properties and s

35 s early after mucosal T. cruzi infection and T. cruzi trans-sialidase vaccination.

36 ammatory monocytes, F4/80(+)macrophages, and T. cruzi tetramer-specific CD8(+) T lymphocytes capable

37 y factors of 110 and 58 against L. major and T. cruzi, with no appreciable toxicity to human osteobla

38 een the shape of the inhibitor molecules and T. cruzi CYP51 active site topology underlies their high

39 so provides cross-protection against another T. cruzi isolate.

40 or recognized specific interactions for anti-T. cruzi antibodies up to a dilution of 1:10,240 and for

41 Thus, dosing schedules for anti-T. cruzi compounds should be determined empirically, and

42 50 as an advanced lead with an improved anti-T. cruzi activity in vitro (IC(50) = 0.079 muM) and an e

43 tion, aiming to improve in parallel its anti-T. cruzi activity (IC(50) = 0.63 muM) and its human meta

44 pen a new avenue for the development of anti-T. cruzi drugs.

45 d orally bioavailable leads with potent anti-T. cruzi activity in vivo.

46 it is ineffective long-term in asymptomatic T. cruzi carriers.

47 In AT, T. cruzi resides inside adipocytes, T. brucei is found i

48 ly significant correlation was found between T. cruzi vertical transmission and a positive PCR result

49 a complex, multi-tissue relationship between T. cruzi infection, Chagas disease, and host glucose hom

50 Additionally, NT-3 specifically blocked T. cruzi infection of the TrkC-NNR5 transfectants and of

51 invasion of primary murine cardiomyocytes by T. cruzi trypomastigotes.

52 We show that host cell entry by T. cruzi mimics a process of plasma membrane injury and

53 foreskin fibroblast (HFF) cells infected by T. cruzi and into its implication to the parasite life c

54 enic mice are protected against infection by T. cruzi and T. gondii, and survive infections that are

55 reciated events in intracellular invasion by T. cruzi and highlight the importance of T cells that re

56 lymphocytes promoted rapid cell invasion by T. cruzi, which also contributed to parasites escaping t

57 ysin protection and metabolic stimulation by T. cruzi, indicating that extracellular cyclophilin may

58 has remained unclear whether TrkC is used by T. cruzi to enter host cells.

59 r, after highly virulent systemic challenge, T. cruzi immune mice lacking T. cruzi-specific B cells f

60 ate and 100% survival, the acute and chronic T. cruzi infection.

61 ications that eventually result from chronic T. cruzi infection.

62 al mechanism of T cell exhaustion in chronic T. cruzi infection.

63 enormous response, these mice fail to clear T. cruzi infection and subsequently develop chronic dise

64 Eleven commercialized T. cruzi infection RDTs were evaluated on a total of 474

65 sely, infants who did not develop congenital T. cruzi infection had higher levels of IFN-gamma than i

66 int-of-care test for detection of congenital T. cruzi infection.

67 etic markers of susceptibility to congenital T. cruzi infection (hereafter, "congenital infection"):

68 e cohort study of 35 infants with congenital T. cruzi infection, of which 15 and 10 infants had been

69 nfants of 476 seropositive women, congenital T. cruzi infection was detected in 38 infants of 35 moth

70 ection against natural oral and conjunctival T. cruzi challenges.

71 The therapeutic vaccine was able to control T. cruzi infection, as evidenced by reduced parasitemia,

72 to, nor detract from, the ability to control T. cruzi infection.

73 TSKB20, TSKB18, or both epitopes controlled T. cruzi infection and developed effector CD8(+) T cells

74 l (1) as an inhibitor of Trypanosoma cruzi ( T. cruzi ), the causative agent of Chagas disease, and t

75 Trypanosoma cruzi (T. cruzi) infection is endemic in Latin America and is b

76 by the protozoan parasite Trypanosoma cruzi (T. cruzi), is an increasing threat to global health.

77 ent and combined treatment protocols to cure T. cruzi infection initiated with susceptible and drug-r

78 One possible reason for the failure to cure T. cruzi infection is that immunodomination by these TS-

79 uppress to very low levels, but do not cure, T. cruzi infection, which is necessary and possibly suff

80 azole 400 mg b.i.d.; or placebo 10 mg b.i.d. T. cruzi deoxyribonucleic acid was detected by RT-PCR at

81 nhibitors of the sterol 14alpha-demethylase (T. cruzi CYP51) enzyme.

82 During T. cruzi invasion to macrophages, superoxide radical (O(

83 elopment and plasticity of Th17 cells during T. cruzi infection.

84 ression in mouse hearts was evaluated during T. cruzi infection by confocal microscopy and flow cytom

85 SOCS2 is expressed during T. cruzi infection, and its expression is partially redu

86 r stimulating .NO production in mphis during T. cruzi infection.

87 ted to IL-10 and TNF-alpha production during T. cruzi infection independently of TLR agonist used (i.

88 development and macrophage responses during T. cruzi infection.

89 t activity among the monocyte subsets during T. cruzi infection.

90 Uninfected infants born to either T. cruzi-infected or uninfected mothers were also evalua

91 ei brucei (EC(50) = 1-15 muM) and eliminated T. cruzi in infected murine cardiomyoblasts (EC(50) = 5-

92 r to benznidazole monotherapy in eliminating T. cruzi parasites measured by real time polymerase chai

93 e stimulates host cell endocytosis, enhances T. cruzi invasion, and restores normal invasion levels i

94 ive activity in a mouse model of established T. cruzi infection after once daily oral dosing for 20 d

95 Here, we examine T. cruzi mitochondrial gene expression in the mammalian

96 ed to potent inhibitors against experimental T. cruzi infection.

97 production of cytokines during experimental T. cruzi infection.

98 We also found that in vitro feeding T. cruzi-infected differentiated human adipocytes with p

99 Fifty T. cruzi peptides predicted to bind a broad range of cla

100 l)quinoline-3-carbonitrile (NEU-924, 83) for T. cruzi and N-(3-chloro-4-((3-fluorobenzyl)oxy)phenyl)-

101 To specifically optimize drug candidates for T. cruzi CYP51 (TcCYP51), we explored the structure-acti

102 stage-specific gene regulation important for T. cruzi virulence.

103 period, all the patients tested negative for T. cruzi DNA on rt-PCR assay beyond day 14, except for 2

104 disease (ChHD), but most are nonspecific for T. cruzi infection.

105 .8% for W1 and 3.6% for W2 were obtained for T. cruzi (W1) and L. infantum antigen (W2) samples in th

106 tter understanding of a critical pathway for T. cruzi biology allowing the identification of novel an

107 receiving benznidazole, tested positive for T. cruzi DNA on rt-PCR assay (P<0.01 for the comparison

108 serological rapid diagnostic tests (RDT) for T. cruzi infection.

109 of children born to mothers seropositive for T. cruzi were compared: 101 had congenital infection, an

110 )-pyrroline-5-carboxylate dehydrogenase from T. cruzi (TcP5CDH) and report here on how this enzyme co

111 uble EF-hand containing pyrophosphatase from T. cruzi (TcVSP) that, depending on the pH and cofactors

112 n, a peptidyl-prolyl isomerase secreted from T. cruzi epimastigotes, binds to and neutralizes the red

113 dem mass spectrometry to heart sections from T. cruzi-infected and uninfected mice.

114 N-gamma) recall response of splenocytes from T. cruzi-infected mice confirmed that 10 of 26 epitopes

115 exhibiting values comparable with those from T. cruzi lysates.

116 enzyme UDP-galactopyranose mutase (UGM) from T. cruzi, which are the first structures of this enzyme

117 Further, T. cruzi-infected iPLA2gamma-knockout (KO) mice had lowe

118 Furthermore, T. cruzi infection of IL-10(-/-) C57BL/6J mice phenocopi

119 cular tools were used to detect and genotype T. cruzi across humans, reservoirs, and insect vectors i

120 on of these peptides in the context of human T. cruzi infection.

121 a decrease in the number of memory cells in T. cruzi-infected SOCS2 KO mice.

122 e of autophagic and programmed cell death in T. cruzi.

123 strated an impairment of cardiac function in T. cruzi-infected SOCS2 KO mice.

124 dium symporter involved in Pi homeostasis in T. cruzi.

125 died mechanism underlying innate immunity in T. cruzi infection is Toll-like receptor (TLR) activatio

126 , MCP-1, and IFN-gamma production induced in T. cruzi-infected infants correlated with parasitemia, w

127 valuated the involvement of inflammasomes in T. cruzi infection and demonstrated that apoptosis-assoc

128 at the membrane protein TcHTE is involved in T. cruzi heme transport, although its specific role rema

129 kade of Gal-3 with N-acetyl-d-lactosamine in T. cruzi-infected mice led to a significant reduction of

130 l as Bcl-2 and CD25 expression were lower in T. cruzi-infected subjects compared with uninfected cont

131 enic activity of benznidazole metabolites in T. cruzi, demonstrate that this can result in multi-drug

132 -0.46% of the proteome is N-myristoylated in T. cruzi approaching that of other eukaryotic organisms

133 Overexpression of PAR4 in T. cruzi enhanced the subdominant PAR4-specific CD8(+) T

134 amma contributes to eicosanoid production in T. cruzi infection.

135 Not all dually acylated proteins in T. cruzi are flagellar, however.

136 route for the secretion of MASP proteins in T. cruzi, which uses EVs as vehicles for immature and mi

137 tagged genes is done to localize proteins in T. cruzi.

138 s flanking the polycistronic units (PTUs) in T. cruzi.

139 by the small trypanosomatid-exclusive RBP in T. cruzi, U-rich RBP 1 (TcUBP1).

140 in eukaryotes, is a promising drug target in T. cruzi.

141 lence factor (prpA in Brucella and tcPrac in T. cruzi) that induces B-cell proliferation and promotes

142 analysis of clathrin-mediated trafficking in T. cruzi, allowing comparison between protein cohorts an

143 ovel biological functions for TcPIWI-tryp in T. cruzi and other members of the trypanosomatid clade.

144 hile an inhibitor of HO-1 activity increased T. cruzi parasitemia in blood.

145 xogenous microvesicles resulted in increased T. cruzi parasitemia.

146 Thus, endogenous Gal-1 may influence T. cruzi infection by fueling tolerogenic circuits that

147 in response to T. cruzi infection, inhibits T. cruzi motility, and plays an important role in reduci

148 ion as key processes that fuel intracellular T. cruzi growth.

149 ey cellular process regulating intracellular T. cruzi growth and illuminate the potential to leverage

150 emic challenge, T. cruzi immune mice lacking T. cruzi-specific B cells failed to control parasitemia

151 came functionally exhausted after high-level T. cruzi systemic challenge.

152 potential to leverage host pathways to limit T. cruzi infection.

153 standing the specialization of the two major T. cruzi strains occurring in the U.S.

154 The two major T. cruzi strains occurring in the U.S. seem to exhibit d

155 Mechanistically, T. cruzi-specific CD8(+) T cells generated in the absenc

156 ffector T cell responses early after mucosal T. cruzi infection and T. cruzi trans-sialidase vaccinat

157 are critical for systemic, but not mucosal, T. cruzi protective immunity.

158 Infection with multiple T. cruzi strains may influence serological diagnostic te

159 Limitations in immune responses to natural T. cruzi infection usually result in parasite persistenc

160 = 60 nM, T. brucei brucei IC(5)(0) = 520 nM, T. cruzi = 7.6 muM), inducing a typical multiple nuclei

161 ns of mice infected with lethal or nonlethal T. cruzi strains and doses.

162 e of infection does not alter the ability of T. cruzi to establish infection in muscle tissue nor doe

163 antitative, spatial, and temporal aspects of T. cruzi infection are central to a fuller understanding

164 n parasite diversity and clinical aspects of T. cruzi infections.

165 we have defined some biosynthetic aspects of T. cruzi mucins, key molecules involved in parasite prot

166 Unusual characteristics of T. cruzi are that it possesses cellular levels of pyroph

167 ins to be fully determined in the context of T. cruzi infection, our data suggest that, under conditi

168 ulatory molecule critical for the control of T. cruzi infection.

169 hich are potent against in vitro cultures of T. cruzi and are greater than 160-fold selective over ho

170 uscle MHC I in mice during the first 20 d of T. cruzi infection resulted in enhanced CD8-dependent re

171 Early diagnosis of T. cruzi infection is crucial.

172 Since the discovery of T. cruzi by Carlos Chagas >100 years ago, much has been

173 nvestigated the transcriptome AS dynamics of T. cruzi (Y strain) infected human foreskin fibroblasts

174 y of both replicative and infective forms of T. cruzi.

175 and resistance, we sequenced the genomes of T. cruzi Y strain (35.5 Mb) and three benznidazole-resis

176 RNA expression profiling data from hearts of T. cruzi infected mice.

177 that peroxynitrite-mediated inactivation of T. cruzi Fe-SODs is due to the site-specific nitration o

178 VNI is a potent experimental inhibitor of T. cruzi sterol 14alpha-demethylase.

179 and persistence benefits to TcI isolates of T. cruzi.

180 We evaluated the serum levels of T. cruzi kinetoplast DNA (TckDNA), T. cruzi 18S ribosoma

181 mic and local responses in a murine model of T. cruzi infection, using knockout animals.

182 Mouse models of T. cruzi infection have been used to study heart damage

183 er once daily oral dosing in mouse models of T. cruzi infection.

184 nslated region (3'-UTR) of a large number of T. cruzi mRNAs that is important for mRNA abundance in t

185 isease pathogenesis; however, the outcome of T. cruzi infection is highly variable and difficult to p

186 The relevance of AhR for the outcome of T. cruzi infection is not known and was investigated her

187 are not effective in altering the outcome of T. cruzi infection, and as RvD1 has been evaluated as a

188 erent events involved in the pathogenesis of T. cruzi infection, contributing to a better overall und

189 therefore participate in the pathogenesis of T. cruzi infection.

190 , the main papain-like cysteine peptidase of T. cruzi, is an important virulence factor and a chemoth

191 itic activity by testing for the presence of T. cruzi DNA, using real-time polymerase-chain-reaction

192 ing 10 had been diagnosed by the presence of T. cruzi-specific Abs at 10-12 mo old.

193 o reduced the intracellular proliferation of T. cruzi amastigotes in infected macrophages in a concen

194 The proportion of T. cruzi-infected infants with clinical signs has fallen

195 at cruzipain, the major cysteine protease of T. cruzi, is responsible for truncating host Apo A-I.

196 eded by the sequestration and replication of T. cruzi in host tissues.

197 ammatory response, promote the resolution of T. cruzi infection, and prevent cardiac fibrosis.

198 ns, host AS events that occur as a result of T. cruzi infection have yet to be explored.

199 Polymerase chain reaction screening of T. cruzi-infected pregnant women is a useful tool for pr

200 he best compounds (64a) cleared all signs of T. cruzi infection in mice when CYP metabolism was inhib

201 trafficking in at least some life stages of T. cruzi may be AP-2-independent.

202 genome increase during culture starvation of T. cruzi for unknown reasons.

203 mice infected with a cardiotropic strain of T. cruzi displayed increased myocarditis and cardiac fib

204 cted with the myotropic Colombiana strain of T. cruzi model many of the immunological and parasitolog

205 caused by the myotropic Colombiana strain of T. cruzi: C3H/HeSnJ (100% mortality, uncontrolled parasi

206 e and in the internal lysosomal structure of T. cruzi.

207 Here we present the x-ray structures of T. cruzi CYP51 in complexes with two alternative drug ca

208 Susceptibility of T. cruzi Fe-SODA toward peroxynitrite was similar to tha

209 Adipose tissue is an early target of T. cruzi infection.

210 reliable vaccine would reduce the threat of T. cruzi infections; however, no suitable vaccine is cur

211 al binding parameters, inhibitory effects on T. cruzi CYP51 activity, and antiparasitic potencies of

212 system, IL-10 production by T cells promotes T. cruzi control and protection from fatal acute myocard

213 for metabolic heterogeneity in recalcitrant T. cruzi infection.

214 ed by a target-based assay using recombinant T. cruzi CYP51.

215 ansgenic mice rapidly responded to secondary T. cruzi infection.

216 onfirmed UDO and UDD as potent and selective T. cruzi CYP51 inhibitors.

217 ry and immune responses in preventing severe T. cruzi-induced disease.

218 Similarly, T. cruzi infection resulted in increased AA and PGE2 rel

219 mature RNA species or editing in the single T. cruzi mitochondrion are linked to differentiation by

220 of analogs against other protozoal species: T. cruzi (Chagas disease), Leishmania major (cutaneous l

221 Profiling of eight stereoisomeric T. cruzi growth inhibitors revealed vastly different in

222 Surprisingly, T. cruzi epimastigotes in replete medium grow at normal

223 ll possible transmission routes for sylvatic T. cruzi.

224 okine receptor CCR5 plays a role in systemic T. cruzi protection.

225 levels of T. cruzi kinetoplast DNA (TckDNA), T. cruzi 18S ribosomal DNA (Tc18SrDNA), and murine mitoc

226 It was concluded that T. cruzi and adenovirus damage the host cell plasma memb

227 They also demonstrate that T. cruzi has a propensity to undergo genetic changes tha

228 In summary, these studies demonstrate that T. cruzi infection activates cardiac myocyte iPLA2gamma,

229 Overall, these results demonstrate that T. cruzi-specific B cells are necessary during systemic,

230 Finally, we demonstrated that T. cruzi epimastigotes can sense intracellular heme by a

231 We discovered that T. cruzi trypomastigotes discard their flagella via an a

232 genomes sequenced from southern Ecuador that T. cruzi in fact maintains truly sexual, panmictic group

233 We found that T. cruzi (Brazil strain) infection of mice results in pa

234 We found that T. cruzi metacyclic trypomastigotes induced microvesicle

235 One key implication of this finding is that T. cruzi may have evolved considerably more recently tha

236 Here, we show that T. cruzi strongly upregulates monocyte chemoattractant p

237 er recent molecular evidence suggesting that T. cruzi evolved from within a broader clade of bat tryp

238 We show for the first time that T. cruzi epimastigotes transitioning from the exponentia

239 Throughout its life cycle, the T. cruzi parasite faces several alternating events of ce

240 redict a hetero-oligomeric structure for the T. cruzi MCU complex, with structural and functional dif

241 e hepatic gluconeogenesis as a cause for the T. cruzi-induced hypoglycemia, despite reduced insulin,

242 hunt for the site of genetic exchange in the T. cruzi life cycle, provides tools to define the geneti

243 4c and show that this chemotype inhibits the T. cruzi CYP51 enzyme, an observation confirmed by X-ray

244 mparative structural characterization of the T. cruzi CYP51 complexes with the three most potent inhi

245 inhibition at the low nanomolar level of the T. cruzi farnesyl diphosphate synthase (TcFPPS).

246 s MG at the N-terminus in one or more of the T. cruzi genomes.

247 drial staining during the main stages of the T. cruzi life cycle.

248 ty appears to be crucial for survival of the T. cruzi parasite in the myriad different environmental

249 lease, microvesicles formed a complex on the T. cruzi surface with the complement C3 convertase, lead

250 A pull-down assay using the T. cruzi component of the prereplication complex Orc1/Cd

251 CD-1 mice infected with the T. cruzi Brazil strain were treated with RvD1.

252 yrosine phosphatase 1 (SHP-1) along with the T. cruzi Tc24 antigen and trans-sialidase antigen 1 (TSA

253 -) mice failed to show any increase in their T. cruzi-specific Th17 response.

254 Thus,T. cruzi infection of mice may be a specific infectious

255 roxyl radical [(HO(2) (*)); pK(a) = 4.8], to T. cruzi at the phagosome compartment.

256 e PCR in the circulation of neonates born to T. cruzi-infected mothers to evaluate the predictive val

257 okines in the circulation of infants born to T. cruzi-infected mothers, which might predict congenita

258 ort a role for microvesicles contributing to T. cruzi evasion of innate immunity.

259 lus fumigatus UGM, which is 45% identical to T. cruzi UGM.

260 terested in better understanding immunity to T. cruzi following oral infection or oral vaccination, k

261 Resistance of Lgals1(-/-) mice to T. cruzi infection was associated with a failure in the

262 and Lec2 also became much more permissive to T. cruzi after transfection with the trkC gene.

263 t is secreted by HCT116 cells in response to T. cruzi infection, inhibits T. cruzi motility, and play

264 y of clinical outcomes and host responses to T. cruzi infection than previously thought, while our mu

265 hat account for the host immune responses to T. cruzi.

266 is critical for regulating Th17 responses to T. cruzi.

267 The MASP multigene family is specific to T. cruzi, accounting for 6% of the parasite's genome and

268 d remarkable activity and selectivity toward T. cruzi epimastigotes and amastigotes.

269 bit cruzain and are exquisitely toxic toward T. cruzi in the intracellular amastigote stage.

270 animal model of infection with a transgenic T. cruzi Y luc strain expressing firefly luciferase, we

271 expression of bacterial PAMPs on transgenic T. cruzi sustains these responses, resulting in enhanced

272 (26.9%) were infected; 31 (6.8%) transmitted T. cruzi to their infants.

273 so inhibited the epimastigotes growth of two T. cruzi strains in vivo.

274 uncovered the features that make UDO and UDD T. cruzi CYP51-specific.

275 Furthermore, we show that upon T. cruzi infection, triple TLR3/7/9(-/-) mice had simila

276 southern super-continent hypothesis, whereby T. cruzi and related parasites evolved in isolation in t

277 The mechanism by which T. cruzi mediates the activation of the ASC/NLRP3 pathwa

278 n these results, we propose a model in which T. cruzi senses intracellular heme and regulates heme tr

279 rated by repeated infectious challenges with T. cruzi.

280 y) mphis were infected for 3 h and 18 h with T. cruzi TcI isolates, SylvioX10/4 (SYL, virulent) and T

281 onary artery endothelial cells (HCAECs) with T. cruzi, suggesting that the absence of iPLA2beta may d

282 Host cells incubated with T. cruzi trypomastigotes are transiently wounded, show i

283 vesicles (EVs) from Vero cells infected with T. cruzi and provide data on the EVs produced by trypoma

284 All infants were infected with T. cruzi discrete typing unit V strain.

285 report that IL-12p35(-/-) mice infected with T. cruzi exhibited a significant increase in Th17 cells

286 lammation in iPLA2beta-KO mice infected with T. cruzi was similar in severity to that in WT mice, but

287 s disease put 8 million people infected with T. cruzi worldwide at risk.

288 y reported that in individuals infected with T. cruzi, apolipoprotein A-I (Apo A-I), the major struct

289 reased in infants congenitally infected with T. cruzi, even before they developed detectable parasite

290 st IgM response in Balb/c mice infected with T. cruzi.

291 animal models and in patients infected with T. cruzi.

292 In addition, in vivo infection with T. cruzi showed a rapid increase of microvesicle levels

293 minants of host resistance to infection with T. cruzi.

294 in resistance to experimental infection with T. cruzi.

295 of host resistance to primary infection with T. cruzi.

296 WT) mice and AhR knockout (AhR KO) mice with T. cruzi (Y strain) and determined levels of parasitemia

297 Infection of C57BL/6 mice with T. cruzi results in up to 40% of all CD8(+) T cells comm

298 oxidizing effector biomolecule, reacted with T. cruzi mitochondrial (Fe-SODA) and cytosolic (Fe-SODB)

299 ses in immunized mice after reinfection with T. cruzi than those in naive mice.

300 In this work, T. cruzi cytosolic Fe-SODB overexpressers (pRIBOTEX-Fe-S