ライフサイエンスコーパス: T. gondii

1 T. gondii (Tg)MIC1-4-6 complex is the most extensively i

2 T. gondii differs substantially in its broad distributio

3 T. gondii established discrete foci of infection in the

4 T. gondii has evolved mechanisms to timely counteract th

5 T. gondii induced CD40 expression both at the transcript

6 T. gondii patatin-like protein 1 (TgPL1) was previously

7 T. gondii tachyzoites are capable of extracting l-Phe(D8

8 We identify 195 T. gondii encoded ligands originating from both secreted

9 We also identify and characterize a T. gondii homologue of Tom7 (TgTom7) that is important f

10 translation initiation site preference for a T. gondii protein.

11 ully used one of these mutants to identify a T. gondii cytoplasmic and conoid-associated protein impo

12 We report the characterization of a T. gondii null mutant for the TgVP1 gene.

13 HhROP5 paralogs increased the virulence of a T. gondii TgROP5 knockout strain.

14 We demonstrate that a T. gondii homologue of Tom22 (TgTom22), a central compon

15 Here we show that a T. gondii mutant with a deletion of the TgPL1 gene (Delt

16 oIL-18) in intestinal epithelial cells after T. gondii or Citrobacter rodentium infection, but also m

17 taining to peptides that are presented after T. gondii infection.

18 any people develop ocular disease soon after T. gondii infection.

19 estigate the ELQ mechanism of action against T. gondii, we demonstrate that endochin and ELQ-271 inhi

20 shows strong antiparasitic activity against T. gondii The same compound inhibits invasion of the mos

21 tion of IgG, IgM, and IgA antibodies against T. gondii in an approximately 1-mul serum or whole-blood

22 R11- and TLR12-mediated host defense against T. gondii.

23 ing more effective, less toxic drugs against T. gondii.

24 sine (NECA) protected CD73(-/-) mice against T. gondii-induced immunopathology, suggesting that the a

25 tion in promoting sterile protection against T. gondii and provide strong evidence for rhoptry-regula

26 ossessed promising activity in vitro against T. gondii.

27 f different isoforms of these enzymes allows T. gondii to rapidly adapt to diverse metabolic requirem

28 ipulation of the host immune response allows T. gondii to not only dampen the ability of the host to

29 Although T. gondii can synthesize sphingolipids de novo, it also

30 13 (3.9%), HSV-1 in 5 (1.5%), and HSV-2 and T. gondii in none.

31 protected against infection by T. cruzi and T. gondii, and survive infections that are lethal to wil

32 of ill children reflecting brain damage and T. gondii infection.

33 red for the egress of both P. falciparum and T. gondii.

34 the genomic synteny between H. hammondi and T. gondii to be >95%.

35 q) to profile the transcriptomes of mice and T. gondii during acute and chronic stages of infection.

36 und that seroprevalence of Brucella spp. and T. gondii antibodies likely increased through time, and

37 We determined if CD40 induces anti-T. gondii activity at the level of nonhematopoietic cell

38 eal that systemic infectious agents, such as T. gondii, can induce long-term immune alterations assoc

39 ecently been shown to play a role in asexual T. gondii daughter cell formation, yet the mechanism is

40 Although an association between T. gondii exposure and prey specialization on marine sna

41 Phe operative during the interaction between T. gondii and its host cell.

42 g imaging flow cytometry, we found that both T. gondii and IL-10 inhibited virus-induced nuclear tran

43 site burdens at secondary sites colonized by T. gondii and succumb to infection.

44 similar functions in host cell engagement by T. gondii.

45 tablishment of infection in the human eye by T. gondii tachyzoites have not been investigated.

46 criptional downregulation of MHC-II genes by T. gondii was previously established, but the precise me

47 Synthesis of a compound set was guided by T. gondii SAR with 1r found to be superior for T. gondii

48 tion was inhibited only in cells infected by T. gondii, which inhibited neither uptake of GFP-HSV nor

49 ics aimed at preventing retinal infection by T. gondii.

50 mechanism of inhibition of TLR signaling by T. gondii and IL-10 and suggest potential negative conse

51 ogenic functions during ileitis triggered by T. gondii, it was required for host defense against C. r

52 so the disrupted gene and protein are called T. gondii Brain Colonization Protein 1 (TgBCP1).

53 innate immune responses to restrict cerebral T. gondii growth.

54 Here we have shown that a chronic T. gondii infection can prevent Plasmodium berghei ANKA-

55 g the early stage of reactivation of chronic T. gondii infection to control tachyzoite growth.

56 oliferate to prevent reactivation of chronic T. gondii infection.

57 1 plays a role in the maintenance of chronic T. gondii infection.

58 cytes that infiltrate the brain upon chronic T. gondii infection, plays a decisive role in host defen

59 human malaria parasite, using a conditional T. gondii ADF-knockout line complemented with ADF varian

60 antigenic recall in infants with congenital T. gondii infection.

61 we determined that ZBP1 functions to control T. gondii growth.

62 Syn-Cre gp130(fl/fl) mice failed to control T. gondii infection and died of necrotizing TE before da

63 es that plays a critical role in controlling T. gondii infection.

64 Thirteen mussels (1.4%) had detectable T. gondii DNA and the presence of T. gondii in mussels w

65 during gestation is made mostly by detecting T. gondii-specific antibodies, including IgG and IgM, in

66 istic insight into the function of different T. gondii aldolases, we first determined the crystal str

67 sion responses to the infection of different T. gondii strains at day 5 after intraperitoneal inocula

68 pared the genomes of 62 globally distributed T. gondii isolates to several closely related coccidian

69 ations regulates their local behavior during T. gondii infection.

70 Similarly, Tregs in the CNS during T. gondii infection are Th1 polarized, as exemplified by

71 es and was not induced in macrophages during T. gondii infection.

72 factors regulating T(H)1 polarization during T. gondii infection identified the T cell-intrinsic TLR

73 ls that regulate IFN-gamma production during T. gondii infection.

74 erefore play an immunomodulatory role during T. gondii infection in mammals.

75 n the metabolic profile of mouse sera during T. gondii infection.

76 lar factors directing robust and rapid early T. gondii-killing mechanisms in the LEW rat.

77 report a novel function of the endolysosomal T. gondii sortilin-like receptor (TgSORTLR), which media

78 here demonstrated that N. caninum expressing T. gondii's GRA15 and ROP16 kinase are biologically acti

79 Extracellular T. gondii secreted approximately 20% of its total PSD ac

80 ban snails are competent transport hosts for T. gondii.

81 Here, we describe a noncanonical pathway for T. gondii infection of macrophages, in which parasites a

82 identify NLRP3 as an inflammasome sensor for T. gondii in primary human peripheral blood cells and to

83 n MHC class II tetramer reagent specific for T. gondii did not recognize Tregs isolated from the CNS.

84 Here we summarize the major strategies for T. gondii genetic manipulation including genetic crosses

85 gondii SAR with 1r found to be superior for T. gondii , also active against Thai and Sierra Leone st

86 Paternal serum samples were tested for T. gondii antibodies with immunoglobulin (Ig) G dye test

87 o (i) validate sensitive molecular tools for T. gondii detection in mussels and (ii) apply optimized

88 cular characterization revealed alleles from T. gondii types I, II/III, X at the B1 locus, and a nove

89 Herein we purify HLA-A*02:01 complexes from T. gondii infected cells and characterize the peptide li

90 Additionally, NK cells isolated from T. gondii-infected Ahr(-/-) mice had impaired expression

91 otected TFF2-deficient (TFF2(-/-)) mice from T. gondii pathogenesis.

92 that whereas neutrophils and monocytes from T. gondii-infected infants display a combination of proi

93 Toxoplasma gondii (T. gondii) is an apicomplexan parasite that can cause ey

94 ph strain of the parasite Toxoplasma gondii (T. gondii), which preferentially invades immunosuppressi

95 plexan protozoan parasite Toxoplasma gondii (T. gondii).

96 vecii (P. jirovecii, pj), Toxoplasma gondii (T. gondii, tg), and Mycobacterium avium (M. avium, ma) a

97 ggest potential negative consequences of HIV/T. gondii coinfection.

98 ons, this study brings novel evidence on how T. gondii has devised a molecular weapon of choice to ta

99 However, T. gondii inhibited IFN-alpha and TNF-alpha produced in

100 the homologous type I or a distinct type II T. gondii genotypes.

101 evels were dramatically increased in type II T. gondii-infected BMdMs compared to type I- or type III

102 Polymerization kinetics of actin in T. gondii lacks both a lag phase and critical concentrat

103 role of CD73 and extracellular adenosine in T. gondii pathogenesis, we infected wild-type (WT) and C

104 protein tagging and purification approach in T. gondii and used it to show that ROP5 complexes with t

105 Optogenetic induction of cAMP in T. gondii affects host-cell invasion, stage-specific exp

106 nzyme in regulation of glucose catabolism in T. gondii.

107 n) is the second major phospholipid class in T. gondii.

108 ow a remarkable low level of conservation in T. gondii.

109 t classic cell-cycle regulators conserved in T. gondii were not detected in the ubiquitinome.

110 ic manipulation tools have been developed in T. gondii over the past 20 years.

111 lling invasion, egress, and cell division in T. gondii, the roles of most of these genes are unexplor

112 al B1 allele that was recently documented in T. gondii-infected carnivores from California.

113 lecular function of mGBP2 and its domains in T. gondii infection is not known.

114 ome sensor NLRP3 and for potassium efflux in T. gondii-induced IL-1beta production.

115 een PKA and PKG pathways to govern egress in T. gondii.

116 est alternative roles for the AHH enzymes in T. gondii, since AAH1 is essential for growth in nondopa

117 hese factors were involved in mRNA export in T. gondii.

118 ranscription of crucial virulence factors in T. gondii.

119 the size distribution of actin filaments in T. gondii in vitro, providing a mechanistic explanation

120 When we expressed these genes in T. gondii, we found that H. hammondi orthologs of TgROP5

121 ded to reveal the functions of many genes in T. gondii.

122 how that the synthesis of the major lipid in T. gondii, phosphatidylcholine (PtdCho), is initiated by

123 (ATP, nucleic acid, proteins, and lipids) in T. gondii, and either of them is sufficient to ensure th

124 emonstrate the critical role ALOX12 plays in T. gondii infection in humans.

125 r the evolution of virulence polymorphism in T. gondii.

126 11 previously undescribed apical proteins in T. gondii and identify an essential component named cono

127 ensive analysis of palmitoylated proteins in T. gondii, identifying a total of 282 proteins, includin

128 skeletal structures differs substantially in T. gondii, the molecular motor dependence of DG traffick

129 prevalence and function of ubiquitination in T. gondii, we mapped the ubiquitin proteome of tachyzoit

130 s of modified CRISPR-Cas9 systems for use in T. gondii, such as regulation of gene expression, labeli

131 a cone-shaped assembly, the conoid, which in T. gondii comprises 14 spirally arranged fibers that are

132 hase (NOS2) (an effector molecule to inhibit T. gondii growth) and the numbers of CD4(+) and CD8(+) T

133 Interestingly, T. gondii infection did not induce an IL-1beta response

134 lted in more efficient control of intestinal T. gondii infection.

135 ance of IRG recruitment to the intracellular T. gondii-containing vacuole, thus protecting the parasi

136 s that contributes to resistance to invading T. gondii, and they thus unveil new avenues for developi

137 oxidative stress as a mechanism for killing T. gondii.

138 poietic compartments contributes to limiting T. gondii-induced immunopathology.

139 he H. hammondi primary sequence of two major T. gondii mouse virulence genes, TgROP5 and TgROP18.

140 regions of increased sentinel marine mammal T. gondii infection.

141 solated from ZBP1 deletion (ZBP1(-/-)) mice, T. gondii has an increased rate of replication and a dec

142 In a mouse model, T. gondii strains can be divided into three groups, incl

143 Monoclonal T. gondii-specific CD8 T cells adoptively transferred in

144 laboratory aquaria, and to test for natural T. gondii contamination in field-collected snails.

145 evealed a high prevalence (29 of 81; 36%) of T. gondii infection in fathers, relative to the average

146 ctivated macrophages, even in the absence of T. gondii infection.

147 ther, structural and biochemical analyses of T. gondii aldolase and aldolase-like proteins reveal div

148 e potential to revolutionize the analysis of T. gondii biology and help us to better develop new drug

149 ylated H4K31 is enriched in the core body of T. gondii active genes but inversely correlates with tra

150 to contribute most to the disease burden of T. gondii, ocular disease from acquired infection was re

151 In the case of T. gondii infection, this self-regulatory pathway is cri

152 In this study, we assess the contribution of T. gondii SPATR (TgSPATR) to T. gondii invasion by genet

153 complex play crucial roles in the control of T. gondii in vitro and in vivo.

154 a role for ZBP1 in assisting host control of T. gondii infection.

155 Control of T. gondii replication by mGBP2 requires GTP hydrolysis a

156 isplay defects in the replication control of T. gondii.

157 amine scaffold interrupts the lytic cycle of T. gondii at submicromolar concentration by targeting AS

158 al to the intracellular replicative cycle of T. gondii including secretion of adhesins, motility, inv

159 lays a role during the normal lytic cycle of T. gondii.

160 o lack of sensitive methods for detection of T. gondii in water, this study utilized an alternative s

161 leting the mitochondrion-associated DHODH of T. gondii (TgDHODH) failed.

162 y platforms, as the serological diagnosis of T. gondii infection does not rely on the detection of a

163 We evaluated the effects of T. gondii infection on survival of our 582 cardiac allog

164 show here that a small-molecule enhancer of T. gondii motility and invasion (compound 130038) causes

165 ecal pellets, snails may facilitate entry of T. gondii into the nearshore marine food web.

166 Amounts of tachyzoite (acute stage form of T. gondii)-specific SAG1 mRNA and numbers of foci associ

167 The growth of T. gondii aldolase crystals in acidic conditions enabled

168 ined lipid synthesis, survival and growth of T. gondii in varying nutritional milieus.

169 This was accompanied by killing of T. gondii dependent on lysosomal enzymes.

170 Accumulation of LAMP-1 and killing of T. gondii were dependent on the autophagy proteins Becli

171 ment epithelial cells resulted in killing of T. gondii.

172 clin 1 to stimulate autophagy and killing of T. gondii.

173 amma effectors onto the vacuolar membrane of T. gondii and its consequent disruption.

174 proteins along the cortical microtubules of T. gondii, established during daughter biogenesis and re

175 ffective in acute and latent mouse models of T. gondii infection, significantly reducing the amount o

176 apeutics, we screened insertional mutants of T. gondii for a reduced ability to form cysts in the bra

177 st but not least, the observed physiology of T. gondii tachyzoites appears to phenocopy cancer cells,

178 detectable T. gondii DNA and the presence of T. gondii in mussels was significantly associated with p

179 OX12 knockdown attenuated the progression of T. gondii infection and resulted in greater parasite bur

180 Proliferation of T. gondii is dependent on its ability to invade host cel

181 lizes at the parasitophorous vacuole (PV) of T. gondii; however, the molecular function of mGBP2 and

182 on and suggest that sustained replication of T. gondii in the gut may be a function of pathogen lumin

183 ncreases by 3-fold during the replication of T. gondii, and soluble phosphatidylserine decarboxylase

184 identify neutrophils as motile reservoirs of T. gondii infection and suggest a surprising retrograde

185 as to measure concentration and retention of T. gondii by marine snails in laboratory aquaria, and to

186 determine the prevalence and genotype(s) of T. gondii in mussels.

187 n ESI + mode and 74 in ESI - mode in sera of T. gondii-infected mice compared to the control mice.

188 hils and other immune cells in the spread of T. gondii infection through the lumen of the intestine.

189 strated that the acute (tachyzoite) stage of T. gondii depends on cooperativity of glucose and glutam

190 ely hardy free-living environmental stage of T. gondii shed in faeces of domestic and wild felids, ar

191 preferentially used by avirulent strains of T. gondii and confers an infectious advantage over virul

192 Strains of T. gondii are globally diverse, with more than 16 distin

193 e infection by type I and type II strains of T. gondii, and this vaccination also severely reduced or

194 ght confer resistance to virulent strains of T. gondii.

195 how that the unusual population structure of T. gondii is characterized by clade-specific inheritance

196 properties may contribute to the success of T. gondii as a human pathogen.

197 ned the regulation of CD40 on the surface of T. gondii-infected bone marrow-derived macrophages (BMdM

198 ich may underlie the promiscuous survival of T. gondii tachyzoites in diverse host cells.

199 ver, TLR11 only modestly affects survival of T. gondii-challenged mice.

200 is context, IFN-gamma activates a variety of T. gondii-targeting activities in immune and nonimmune c

201 g macrophage survival and acute virulence of T. gondii in mice.

202 rovide broad-based functional information on T. gondii genes and will facilitate future approaches to

203 agocytes, which dictated the outcome of oral T. gondii infection in mice.

204 py in conjunction with a mouse model of oral T. gondii infection to address this issue.

205 manifestations were associated with paternal T. gondii infection status.

206 lack the parasite, or that have phagocytosed T. gondii.

207 n of JNK, CaMKKbeta, AMPK, or ULK1 prevented T. gondii killing in CD40-activated macrophages.

208 However, prior T. gondii infection blocks IFN-gamma-dependent gene tran

209 ected role of phagocytic cells in processing T. gondii oocysts, in line with non-classical routes of

210 applied as a method for confirming putative T. gondii oocysts detected in snail faeces and tissues b

211 revalence of chronic and incidence of recent T. gondii infections in fathers of congenitally infected

212 Toll-like receptor 11 (TLR11) recognizes T. gondii profilin (TgPRF) and is required for interleuk

213 Functionally, mGBP2 reduces T. gondii proliferation because mGBP2-deficient cells di

214 , 8.2 chain have a potent activity to remove T. gondii cysts from the brain.

215 activate CD8(+) T cells capable of removing T. gondii cysts.

216 demonstrate higher than previously reported T. gondii contamination of California coastlines, and de

217 Treatment with soluble T. gondii antigens (STAg) reduced parasite sequestration

218 Upon stimulation, T. gondii-infected ZBP1(-/-) macrophages display increas

219 s to facilitate drug development: EGS strain T. gondii forms cysts in vitro that induce oocysts in ca

220 Surprisingly, T. gondii ligands are significantly longer than uninfect

221 We now have identified TgIST (T. gondii inhibitor of STAT1 transcriptional activity) a

222 We demonstrate that T. gondii tachyzoites possess regulatory volume decrease

223 Here, we demonstrate that T. gondii Tic22 is an apicoplast-localized protein, esse

224 fluorescence microscopy, we determined that T. gondii invaded but did not induce IFN-alpha or TNF-al

225 Taken together, our results indicate that T. gondii suppresses pDC activation by mimicking IL-10's

226 ongenitally infected children indicates that T. gondii infections cluster within families in North Am

227 It has long been known that T. gondii interferes with major histocompatibility compl

228 Thus our results reveal that T. gondii relies on host-derived sphingolipids for its d

229 Herein, we show that T. gondii cathepsin B protease (TgCPB) does not undergo

230 Recently, we showed that T. gondii harbors a novel AMA designated as TgAMA4 that

231 The T. gondii genome contains one UCS family myosin co-chape

232 The T. gondii genome encodes six members of the patatin-like

233 LQ-271 inhibit cytochrome c reduction by the T. gondii cytochrome bc(1) complex at 8 nM and 31 nM, re

234 onary implications of these findings for the T. gondii host-pathogen relationship and for human disea

235 ntify an intrinsic role for autophagy in the T. gondii parasite and its close relatives.

236 as partially reversed by a deficiency in the T. gondii-derived ROP16 kinase, known to directly phosph

237 acting as inhibitors of the Q(i) site of the T. gondii cytochrome bc(1) complex.

238 e structure and chemistry of the wall of the T. gondii oocyst by combining wall surface treatments, f

239 echanics in maintaining the integrity of the T. gondii oocysts in the environment or after exposure t

240 cin A1 , suggesting that either TgVP1 or the T. gondii V-H(+) -ATPase (TgVATPase) are sufficient to s

241 We further demonstrate that the T. gondii armadillo repeats-only protein (TgARO) mutant,

242 palmitoylation is ubiquitous throughout the T. gondii proteome and reveal insights into the biology

243 ficient and essential for recruitment to the T. gondii PV.

244 BALB/c mice experimentally infected with the T. gondii Pru strain (Genotype II).

245 Confirming this, T. gondii tachyzoites formed fewer cysts following alkal

246 Thus, T. gondii PTMs are implicated as critical regulators of

247 vealed that TLR11 and TLR12 directly bind to T. gondii profilin and are capable of forming a heterodi

248 efractoriness of LEW rat peritoneal cells to T. gondii infection, resulting in proliferation of paras

249 n found to infect humans and, in contrast to T. gondii, is highly attenuated in mice.

250 Additionally, the odds of exposure to T. gondii were greater for bears that used land than for

251 Following exposure to T. gondii-containing seawater, oocysts were detected by

252 rd the hypothesis that sustained immunity to T. gondii requires repeated antigenic stimulations.

253 R11, TLR12-deficient mice succumb rapidly to T. gondii infection.

254 se domain regulates efficient recruitment to T. gondii in response to IFN-gamma.

255 critical for susceptibility or resistance to T. gondii infection in rats.

256 -12p40), which is required for resistance to T. gondii.

257 he Lewis (LEW) rat is extremely resistant to T. gondii infection.

258 ion of how human cells detect and respond to T. gondii.

259 od-producing innate cytokines in response to T. gondii and demonstrate an unappreciated requirement f

260 here is a common gene expression response to T. gondii infection in mice.

261 ls neither provided a protective response to T. gondii infection nor mediated autoimmune colitis.

262 IL-1beta cleavage and release in response to T. gondii infection, without affecting the release of TN

263 levels of IL-2 in the secondary response to T. gondii, and a blocking of IL-2 signaling by anti-IL-2

264 s critical for the innate immune response to T. gondii, and this TLR may promote host resistance by t

265 est that ALOX12 influences host responses to T. gondii infection in human cells.

266 mma production in the secondary responses to T. gondii, suggesting an importance of induction of CD8(

267 Similar to T. gondii, the HhROP5 locus is expanded, and two distinc

268 ice reveal a marked immune susceptibility to T. gondii.

269 R11-deficient mice are highly susceptible to T. gondii infection, recapitulating the phenotype of 3d

270 contribution of T. gondii SPATR (TgSPATR) to T. gondii invasion by genetically ablating it and restor

271 - 20 nM), and selectivity versus a wild-type T. gondii strain (200-fold).

272 Here, we characterized a unique T. gondii homologue of mammalian lecithin:cholesterol ac

273 f IL-22 in innate lymphoid cells (ILCs) upon T. gondii infection.

274 e T cells in their secondary responses using T. gondii-specific CD8(+) T cell hybridomas and splenic

275 Virulent T. gondii strains secrete kinases and pseudokinases that

276 There was no evidence of West Nile virus, T. gondii, or Brucella spp. in any of the brain tissue s

277 nantly proinflammatory profile upon in vitro T. gondii stimulation.

278 stitute the lytic cycle, as well as the ways T. gondii manipulates host cells to ensure its survival.

279 ial-agglutination and IgG avidity tests when T. gondii IgG and IgM results were positive and serum sa

280 The AIC strongly support models in which T. gondii cysts grow at a constant rate such that the pe

281 investigated the impact of coinfection with T. gondii on the innate virus-directed responses of huma

282 genous IL-2 was provided in combination with T. gondii Ags.

283 ced immunological phenotypes consistent with T. gondii strains.

284 signaling as well as immune experience with T. gondii.

285 uman population is chronically infected with T. gondii cysts, the dormant form of the parasite.

286 Unexpectedly, T-bet(-/-) mice infected with T. gondii develop a strong NK cell IFN-gamma response th

287 umbers of DCs, Flt3L(-/-) mice infected with T. gondii displayed an expansion of CD8alpha(+) and CD11

288 ntervention to combat chronic infection with T. gondii by targeting the persistent cysts of the paras

289 a better understanding of how infection with T. gondii impacts the customized structures required for

290 s were able to prevent lethal infection with T. gondii in the mouse model.

291 hology during intraperitoneal infection with T. gondii than WT mice.

292 On infection with T. gondii, Syn-Cre gp130(fl/fl) mice failed to control T

293 onic toxoplasmosis after oral infection with T. gondii.

294 nt to prevent reactivation of infection with T. gondii.

295 responses to control cerebral infection with T. gondii.

296 helium is increased following infection with T. gondii.

297 vivo, rather than cellular interactions with T. gondii that result in infection, infection and cleara

298 ected wild-type (WT) and CD73(-/-) mice with T. gondii cysts systemically by the intraperitoneal (i.p

299 st cell completely replaces the l-Phe within T. gondii tachyzoites 7-9 hours after infection.

300 e LEW rat versus the BN rat, with or without T. gondii infection, in order to unravel molecular facto