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 clearance in and survival of IFNAR(-/-) mice we

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

4 T. cruzi induced differential polarization of immunoregu

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

6 T. cruzi infection enhanced tissue expression of MBL bot

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

8 T. cruzi proline racemase (TcPRAC), a T. cruzi B-cell mi

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

15 T. cruzi proline racemase (TcPRAC), a T. cruzi B-cell mitogen, may contribute to this dysfunct

16 Acute T. cruzi infection results in polyclonal B-cell activati

17 TSKD14 peptide effectively controlled acute T. cruzi infection.

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

19 IFN-responsive genes are evident early after T. cruzi infection of host cells, we examined the influe

20 asite control and heightened mortality after T. cruzi, L. major, and Toxoplasma gondii infection, des

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

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

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

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 major, L. tarentolae, Trypanosoma brucei and T. cruzi.

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

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

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

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

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

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

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

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

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

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

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

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

48 Antibody to TrkC blocked T. cruzi infection of the TrkC-NNR5 transfectants and of

49 of sialic acid recognition, mediating broad T. cruzi infection both in vitro and in vivo.

50 ophin-3 (NT-3) receptor TrkC is activated by T. cruzi surface trans-sialidase, also known as parasite

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 tory responses in cardiomyocytes infected by T. cruzi and provide a clue to the pathomechanism of sus

54 systems, and in nonneural cells infected by T. cruzi, including cardiac and gastrointestinal muscle

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

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

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

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

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

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

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

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

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

64 d for any infection, most mice fail to clear T. cruzi and subsequently develop chronic disease.

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

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

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

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

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

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

71 ith TS plus CpG protect against conjunctival T. cruzi challenge, limiting local parasite replication

72 ides to induce immunity against conjunctival T. cruzi challenge.

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

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

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

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

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

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

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

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

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

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

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

84 9sv/ev mice were infected with two different T. cruzi strains under lethal and sublethal conditions a

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

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

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

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

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

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

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

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 ed to potent inhibitors against experimental T. cruzi infection.

96 production of cytokines during experimental T. cruzi infection.

97 response in shaping outcomes in experimental T. cruzi infection, groups of wild-type (WT) and type I

98 erefore generated T. brucei lines expressing T. cruzi topoisomerase-II truncated at the carboxyl term

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

100 inant TSKB18-specific CD8+ T cells following T. cruzi infection.

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

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

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

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

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

108 d also be convenient to deliver vaccines for T. cruzi by the oral route, particularly live parasite v

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

110 expression of the corresponding enzyme from T. cruzi.

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 We generated T. cruzi transfectants expressing the N-terminal 24 or 1

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

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

122 es mellitus may have adverse consequences in T. cruzi infection.

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

124 ession of the TcPOT1.1 and TcPOT1.2 genes in T. cruzi epimastigotes revealed that TcPOT1.1 and TcPOT1

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

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

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

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

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

130 for correct plasma membrane localization in T. cruzi epimastigotes or amastigotes.

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

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

133 -0.46% of the proteome is N-myristoylated in T. cruzi approaching that of other eukaryotic organisms

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

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

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

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

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

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

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 oteins that mediate polyamine transport into T. cruzi, as well as most eukaryotes, however, have by-i

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

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

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

152 In contrast, under conditions of lethal T. cruzi challenge, WT mice succumbed to infection where

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

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

155 The development of inhibitors of the major T. cruzi cysteine protease, cruzain, has been demonstrat

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

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

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

159 anism by which lysosomal exocytosis mediates T. cruzi internalization remains unclear.

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

161 reting cells, and significantly less mucosal T. cruzi protection, confirming an important role for CC

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

163 = 60 nM, T. brucei brucei IC(5)(0) = 520 nM, T. cruzi = 7.6 muM), inducing a typical multiple nuclei

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

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

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

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

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

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

170 CD8+ T cells are critical for control of T. cruzi infection, and CD8+ T cells recognizing the imm

171 t role for CCL5 in optimal immune control of T. cruzi replication at the point of initial mucosal inv

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

173 expression during the developmental cycle of T. cruzi, the first immediately after differentiation of

174 Early diagnosis of T. cruzi infection is crucial.

175 that T-bet regulates the differentiation of T. cruzi-specific Th17 cells in vivo in a T cell-intrins

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

177 secreted by the metacyclic infective form of T. cruzi, AgC10, is able to interfere with L-selectin-me

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 We show here that atraumatic placement of T. cruzi in the mouse nasal cavity produced low parasite

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

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

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

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

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

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

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

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

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

203 onse triggered by three different strains of T. cruzi at a local infection site, changes in host gene

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

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

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

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

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

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

210 establishment of infection, by the protozoan T. cruzi.

211 ased mucosal inflammatory responses, reduced T. cruzi-specific Ab-secreting cells, and significantly

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

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

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

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

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

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

218 ll possible transmission routes for sylvatic T. cruzi.

219 antigen protect against gastric and systemic T. cruzi challenge.

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

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

222 We conclude that T. cruzi-mediated mtROS provide primary stimulus for PAR

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

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

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

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

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

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

229 We found that T. cruzi metacyclic trypomastigotes induced microvesicle

230 We show here that T. cruzi binds TrkC, a neurotrophic receptor expressed b

231 Our data indicate that T. cruzi induces broad modulations of the host cell mach

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

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

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

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

236 t (PBN + BZ) was beneficial in arresting the T. cruzi-induced inflammatory and oxidative pathology an

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

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

239 4c and show that this chemotype inhibits the T. cruzi CYP51 enzyme, an observation confirmed by X-ray

240 ly identified as a TrkA ligand, mediates the T. cruzi-TrkC interaction.

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

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

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

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

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

246 POT1.1 and TcPOT1.2 as key components of the T. cruzi polyamine transport pathway, an indispensable n

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

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

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

250 Thus, T. cruzi might exploit an additional neurotrophic recept

251 Thus, T. cruzi subverts the ASM-dependent ceramide-enriched en

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

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

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

255 reduces the susceptibility of host cells to T. cruzi invasion.

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

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

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

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

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

261 N93B1-dependent TLR(s) on host resistance to T. cruzi.

262 ell line (PC12-NNR5) relatively resistant to T. cruzi became highly susceptible to infection when ove

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

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

271 (26.9%) were infected; 31 (6.8%) transmitted T. cruzi to their infants.

272 .1 and TcPOT1.2, encoded by alleles from two T. cruzi haplotypes.

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 hat intranasal immunizations with the unique T. cruzi trans-sialidase (TS) antigen protect against ga

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

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

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

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 Sprague-Dawley rats were infected with T. cruzi and treated with phenyl-alpha-tert-butylnitrone

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

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

287 NSE-Rb db/db mice were infected with T. cruzi to determine the impact of the lack of leptin s

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

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

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

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

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

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

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

295 in resistance to experimental infection with T. cruzi.

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

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

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

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

300 s provides protection against wild-type (WT) T. cruzi challenge.