ライフサイエンスコーパス: Toxoplasma

1 , Zika virus, brucella, cytomegalovirus, and toxoplasma).

2 on support conservation of this mechanism in Toxoplasma.

3 uced clearance of vacuolar pathogens such as Toxoplasma.

4 t associated with the conoid in apicomplexan Toxoplasma.

5 kine secretion in human monocytes exposed to Toxoplasma.

6 exans such as TRAP in Plasmodium and MIC2 in Toxoplasma.

7 elated Plasmodium spp. is also functional in Toxoplasma.

8 member, localizes to the plasma membrane of Toxoplasma.

9 mong the major myeloid cells that respond to Toxoplasma, a ubiquitous foodborne that infects >= 1 bil

10 includes malaria parasites (Plasmodium) and Toxoplasma, achieve remarkable speeds of directional cel

11 n gamma (IFNgamma) elicits a variety of anti-Toxoplasma activities in macrophages.

12 osyltransferase Gat1 is specific for Skp1 in Toxoplasma and also in another protist, the crop pathoge

13 al role in the early immune response against Toxoplasma and are the cell type preferentially infected

14 Toxoplasma and Cryptosporidium infect millions of people

15 that have illuminated the interfaces between Toxoplasma and host and how these interactions control p

16 n at the parasitophorous vacuole employed by Toxoplasma and host, leading to the intricate balance of

17 e that, despite their different host ranges, Toxoplasma and Neospora use a conserved mechanism to co-

18 gress on this realm has come from studies in Toxoplasma and Plasmodium of their respective kinomes an

19 In addition, comparative analysis between Toxoplasma and Plasmodium scRNA-seq results reveals conc

20 and therefore parasite proliferation in both Toxoplasma and Plasmodium.

21 racterize an important chaperone-like GRA in Toxoplasma and provide a resource for the community to f

22 ach to study protein-protein interactions in Toxoplasma and provides the first insight into the archi

23 The substitution of glycosyltransferases in Toxoplasma and Pythium by an unrelated bifunctional enzy

24 ms involved in mitochondrial distribution in Toxoplasma and the consequences of these mitochondrion c

25 the genera Plasmodium, Cryptosporidium, and Toxoplasma and those of the relatively understudied zoon

26 picoplast inheritance in both Plasmodium and Toxoplasma, and additionally mediates efficient cytokine

27 ely related to parasites such as Plasmodium, Toxoplasma, and Cryptosporidium, which are causing sever

28 with a focus on three parasites: Plasmodium, Toxoplasma, and Cryptosporidium.

29 oan parasites such as Plasmodium, Entamoeba, Toxoplasma, and Leishmania secrete an inflammatory macro

30 eospora caninum, which is closely related to Toxoplasma but has a restricted host range and uses diff

31 Toxoplasma can reach distant organs, especially the brai

32 Toxoplasma can reside in the brain for extensive periods

33 One route by which Toxoplasma co-opts its host cell is through hijacking ho

34 These select BKIs include anti-Toxoplasma compounds that are effective against acute ex

35 d local intensity measurements of F-actin in Toxoplasma conditional mutants revealed molecular determ

36 in the gut of its definitive host, felines, Toxoplasma converts into gametocytes that produce infect

37 nic infection with the apicomplexan parasite Toxoplasma correlates with certain neurological disorder

38 cluding human pathogens, such as Plasmodium, Toxoplasma, Cryptosporidium and Babesia species.

39 However, murine innate recognition of toxoplasma depends on the interaction of parasite profil

40 Mechanistically, GBP1 promoted Toxoplasma detection by AIM2, which induced GSDMD-indepe

41 ovides a genetic switch to study and control Toxoplasma differentiation and will inform prevention an

42 We focus on TgWIP, whose deletion affects Toxoplasma dissemination to distant organs.

43 y, GBP1 could be bypassed by the delivery of Toxoplasma DNA or bacterial LPS into the cytosol, pointi

44 Thus, we have identified how the Toxoplasma effector GRA15 affects cell-autonomous immuni

45 ceptibility to human IFNgamma exist, but the Toxoplasma effector(s) that determine these differences

46 8 exhaustion has been previously reported in Toxoplasma encephalitis (TE)-susceptible model, our curr

47 ional responses that underpin human monocyte-Toxoplasma encounters at the single cell level.

48 However, the Toxoplasma enzyme catalyzes formation of a Galalpha1,3Gl

49 Furthermore, we report that Toxoplasma-exposed and unexposed monocytes are transcrip

50 we use focused CRISPR libraries to identify Toxoplasma genes that affect in vivo fitness.

51 community to further explore the function of Toxoplasma genes that determine fitness in IFNgamma-acti

52 a genome-wide CRISPR screen we identify 353 Toxoplasma genes that determine parasite fitness in naiv

53 e a framework for systemic identification of Toxoplasma genes with in vivo effects at the site of inf

54 The Toxoplasma genome encodes a suite of likely glycogenes e

55 d that, despite the sequence difference, the Toxoplasma glycan still assumes an ordered conformation

56 Toxoplasma glycans resemble those of other eukaryotes, b

57 uoles, but like nearly all other eukaryotes, Toxoplasma glycosylates many cellular proteins and lipid

58 of different sizes in the protozoan parasite Toxoplasma gondi and describe optimised analysis methods

59 ases of invasive protozoal infections due to Toxoplasma gondii (n = 3), Trypanosoma cruzi, and Leishm

60 tudies have reported elevated levels of anti-Toxoplasma gondii (T. gondii) antibodies in patients wit

61 positive Goldmann-Witmer coefficient (GWC), Toxoplasma gondii (T. gondii) immunoblot, or T. gondii-s

62 Toxoplasma gondii (T. gondii) is a protozoan parasite th

63 c cells infected with the protozoan parasite Toxoplasma gondii (Tg).

64 In Dictyostelium (a social amoeba), Toxoplasma gondii (the agent for human toxoplasmosis), a

65 derstanding how immunity is elicited against Toxoplasma gondii - a complex pathogen with multiple mec

66 , deletion of the dpy19 gene in the parasite Toxoplasma gondii abolished C-mannosyltransferase activi

67 al pH, was cryotrapped in the active site of Toxoplasma gondii aldolase crystals to high resolution.

68 ocytosis operates during gliding motility in Toxoplasma gondii and appears to be crucial for the esta

69 target of actinonin in the related parasite Toxoplasma gondii and implicated P. falciparum FtsH1 as

70 ch as Plasmodium species that cause malaria, Toxoplasma gondii and kinetoplastid protozoa, including

71 hree protozoan parasites (Trypanosoma cruzi, Toxoplasma gondii and Leishmania major), in which the Gz

72 hallenge with the common coccidian parasites Toxoplasma gondii and Neospora caninum activated GABAerg

73 zes to the apical pole in invasive stages of Toxoplasma gondii and Plasmodium berghei, and apical pos

74 is review primarily focuses on studies using Toxoplasma gondii and Plasmodium spp. as the best studie

75 Apicomplexan parasites Toxoplasma gondii and Plasmodium spp. use latent stages

76 Using Toxoplasma gondii and Salmonella enterica Typhimurium we

77 The apical complex of Toxoplasma gondii and some other apicomplexans includes

78 expansion microscopy (U-ExM) to localize the Toxoplasma gondii Apical Cap protein 9 (AC9) and its par

79 ost effects caused by the protozoan parasite Toxoplasma gondii are poorly understood.

80 Here, we use Toxoplasma gondii as a model system to functionally char

81 Here we establish that Toxoplasma gondii aspartyl protease 3 (ASP3) resides in

82 rmation of naturally occurring peptides from Toxoplasma gondii bound by HLA-A*02:01.

83 function of the motility apparatus of living Toxoplasma gondii by adhering a microsphere to the surfa

84 tance to the intracellular vacuolar pathogen Toxoplasma gondii by inducing the destruction of the par

85 ) have been shown to be potent inhibitors of Toxoplasma gondii calcium-dependent protein kinase 1.

86 It has been proposed that Toxoplasma gondii can cross biological barriers as a mot

87 the asexual cycle of the protistan parasite Toxoplasma gondii can occur in any warm-blooded mammal,

88 hronic infection with the protozoan parasite Toxoplasma gondii causes a nonresolving Th1 myositis wit

89 The apicomplexan parasite Toxoplasma gondii causes macrophage death through uniden

90 oplasmosis, pyrazolopyrimidine inhibitors of Toxoplasma gondii CDPK1 demonstrated in vitro and in viv

91 Toxoplasma gondii chronically infects a quarter of the w

92 Upon infection, the intracellular parasite Toxoplasma gondii co-opts critical functions of its host

93 s left eye due to varicella-zoster virus and Toxoplasma gondii coinfection documented by polymerase c

94 itis secondary to varicella-zoster virus and Toxoplasma gondii coinfection in a male patient in Bogot

95 Toxoplasma gondii contains a limited subset of actin bin

96 The Toxoplasma gondii cyst stage is resistant to drug therap

97 The protozoan parasite Toxoplasma gondii develops within a parasitophorous vacu

98 Toxoplasma gondii DNA detection is essential to antenata

99 contribution of each gene from the parasite Toxoplasma gondii during infection of human fibroblasts.

100 ts of the Ca(2+) signaling pathway dictating Toxoplasma gondii egress have been identified, whether t

101 When Toxoplasma gondii egresses from the host cell, glycerald

102 Toxoplasma gondii encodes three protein kinase A catalyt

103 n of subtelomeric virulence genes, while the Toxoplasma gondii genome was dominated by clustering of

104 ing a synthetic phosphoglycan portion of the Toxoplasma gondii glycosylphosphatidylinositol (GPI1) fo

105 uous supply of potent killer T cells to curb Toxoplasma gondii growth during latency.

106 Here, we demonstrate that the apicomplexan Toxoplasma gondii harbors homologues of proteins from al

107 Toxoplasma gondii has been taken as an example for this

108 Traditionally, the protozoan parasite Toxoplasma gondii has been thought of as relevant to pub

109 The obligate intracellular parasite Toxoplasma gondii has unusually stable cortical microtub

110 Apicomplexan parasites like Toxoplasma gondii have a specialized cilium-like structu

111 study evaluated the usefulness of adding the Toxoplasma gondii IgA antibody enzyme-linked immunosorbe

112 ly intrinsically disordered component of the Toxoplasma gondii IMC, as essential for apical complex d

113 sive neurocognitive assessments and had anti-Toxoplasma gondii immunoglobulin G (anti-Toxo IgG) measu

114 e Ca(2+) signaling in the model apicomplexan Toxoplasma gondii In doing so, we took advantage of the

115 that produce strong immune responses against Toxoplasma gondii in HLA supermotif, transgenic mice.

116 lator of autophagy and autophagic killing of Toxoplasma gondii in host cells.

117 Brain infection by the parasite Toxoplasma gondii in mice is thought to generate vulnera

118 Studies in Plasmodium spp. and Toxoplasma gondii in particular have revealed that these

119 ter, cytomegalovirus, Epstein-Barr virus and Toxoplasma gondii in patients with uveitis.

120 nd that the intracellular protozoan parasite Toxoplasma gondii induced an early IL-1beta response (wi

121 Toxoplasma gondii infection causes substantial morbidity

122 Here, we describe Toxoplasma gondii infection converts NK cells into ILC1-

123 Toxoplasma gondii infection in mice provides an excellen

124 The course of Toxoplasma gondii infection in rats closely resembles th

125 Toxoplasma gondii infection is an asymptomatic disease,

126 Intrinsic to Toxoplasma gondii infection is the parasite-induced modu

127 An early hallmark of Toxoplasma gondii infection is the rapid control of the

128 er they develop these characteristics during Toxoplasma gondii infection is unknown.

129 the epigenomic and transcriptomic effects of Toxoplasma gondii infection on human host cells and demo

130 in NK cells both in vitro and in a model of Toxoplasma gondii infection revealed de novo chromatin a

131 of processes related to the establishment of Toxoplasma gondii infection, such as the formation of th

132 f granulocyte responses and pathology during Toxoplasma gondii infection.

133 new insights into the roles of CDPKs during Toxoplasma gondii infection.

134 responses using a mouse model for persistent Toxoplasma gondii infection.

135 The most common method to diagnose Toxoplasma gondii infections is the serological determin

136 The intracellular parasite Toxoplasma gondii infects nucleated cells in virtually a

137 The Toxoplasma gondii inner membrane complex (IMC) is an imp

138 ined the effects of endothelial cell CD40 on Toxoplasma gondii invasion of the retina and brain, orga

139 Toxoplasma gondii is a classic model for studying obliga

140 Toxoplasma gondii is a common parasite of humans and ani

141 Toxoplasma gondii is a common protozoan parasite that in

142 d control of HIV type 1 replication, whereas Toxoplasma gondii is a life-threatening opportunistic in

143 Infection with the protozoan parasite Toxoplasma gondii is a major health risk owing to birth

144 Toxoplasma gondii is a protist parasite of warm-blooded

145 Toxoplasma gondii is a remarkably successful protozoan p

146 Toxoplasma gondii is a ubiquitous, obligate intracellula

147 Toxoplasma gondii is a widespread parasite with consider

148 Toxoplasma gondii is a widespread parasitic pathogen tha

149 Toxoplasma gondii is a widespread protozoan parasite inf

150 The propagation of Toxoplasma gondii is accomplished by repeated lytic cycl

151 Toxoplasma gondii is among the most prevalent parasites

152 Toxoplasma gondii is an incredibly successful parasite o

153 Toxoplasma gondii is an intracellular parasite that caus

154 Toxoplasma gondii is an intracellular parasite that caus

155 Toxoplasma gondii is an intracellular parasite that is h

156 Toxoplasma gondii is an obligate intracellular parasite

157 Toxoplasma gondii is an obligate intracellular parasite

158 Toxoplasma gondii is an obligate protozoan parasite that

159 Toxoplasma gondii is an obligate, intracellular eukaryot

160 Toxoplasma gondii is an opportunistic infection that can

161 Toxoplasma gondii is associated with physiological and p

162 Toxoplasma gondii is associated with physiological effec

163 Toxoplasma gondii is considered to be one of the most su

164 ted target of actinonin in P. falciparum and Toxoplasma gondii is FtsH1, a homolog of a bacterial mem

165 Unlike its animal counterparts, Skp1 from Toxoplasma gondii is hydroxylated by an O2-dependent pro

166 CD40-mediated autophagic killing of Toxoplasma gondii is known to require TNF-alpha.

167 The protozoan parasite Toxoplasma gondii is thought to exploit monocyte traffic

168 In mice, infection with Toxoplasma gondii leads to a Th1-polarized parasite-spec

169 The protozoan parasite Toxoplasma gondii lives inside a vacuole in the host cyt

170 ve genome-scale metabolic model (GEM) of the Toxoplasma gondii metabolic network that incorporates ge

171 Horizontal transmission of Toxoplasma gondii occurs primarily via ingestion of envi

172 deliver a double punch that can destroy the Toxoplasma gondii parasite and its niche inside cells.

173 Toxoplasma gondii parasites rapidly exit their host cell

174 Apicomplexan parasites such as Toxoplasma gondii possess an unusual heme biosynthesis p

175 Toxoplasma gondii possesses a limited set of actin-regul

176 The intracellular parasite Toxoplasma gondii possesses three distinct Drps.

177 The Toxoplasma gondii PV is filled with a network of tubulat

178 Toxoplasma gondii reaches the CNS by circulating in bloo

179 Apicomplexan parasites such as Toxoplasma gondii rely on a unique form of locomotion kn

180 The obligate intracellular parasite Toxoplasma gondii replicates in an unusual process, desc

181 ability, the obligate intracellular parasite Toxoplasma gondii reprograms its metabolism.

182 l of chronic CNS infection with the parasite Toxoplasma gondii requires ongoing T cell responses in t

183 TRIM21 as a previously unknown modulator of Toxoplasma gondii resistance in vivo thereby extending h

184 GPI1 in combination with SAG1 may strengthen Toxoplasma gondii serology, in particular in seroepidemi

185 n infection caused by the protozoan parasite Toxoplasma gondii that can lead to severe sequelae in th

186 social amoeba Dictyostelium and the parasite Toxoplasma gondii The full effect of hydroxylation requi

187 -scale CRISPR screens recently developed for Toxoplasma gondii to discover sensitizing and desensitiz

188 Rodents are critical for the transmission of Toxoplasma gondii to the definitive feline host via pred

189 f intracellular proteins, the human pathogen Toxoplasma gondii transfers a different sugar, fucose, t

190 It is believed that infection by Toxoplasma gondii triggers a lifelong protective immunit

191 re we describe the myristoylated proteome of Toxoplasma gondii using chemoproteomic methods and show

192 mice responded to the intracellular parasite Toxoplasma gondii While the loss of IL-27p28 and its ove

193 re infected with the intracellular protozoan Toxoplasma gondii(1).

194 ith potential pathogens (West Nile virus and Toxoplasma gondii) and one with Streptococcus species wi

195 Toxoplasma gondii, a common neurotropic parasite, is inc

196 switch between the lytic and latent forms of Toxoplasma gondii, a parasite that causes a persistent b

197 Toxoplasma gondii, a protozoan parasite, undergoes a com

198 ook advantage of the genetic tractability of Toxoplasma gondii, a related parasite that shows moderat

199 The cytoskeleton of Toxoplasma gondii, an important human parasite, contains

200 Toxoplasma gondii, an obligate intracellular protozoan p

201 thogen challenges, including H1N1 influenza, Toxoplasma gondii, and Ebola virus.

202 ovirus, herpes simplex virus, rubella virus, Toxoplasma gondii, and Zika virus.

203 lium discoideum, and the protozoan parasite, Toxoplasma gondii, both lacking HIF.

204 ior exposure to the pathogens Brucella spp., Toxoplasma gondii, Coxiella burnetii, Francisella tulare

205 ng fluorescent proteins or targeted genes of Toxoplasma gondii, driven by N. caninum promoters, have

206 A particular emphasis is placed on Toxoplasma gondii, during both its acute and latent stag

207 In Toxoplasma gondii, extracellular potassium levels and ot

208 e knockout screens in Plasmodium berghei and Toxoplasma gondii, in which pooled transfections of mult

209 Toxoplasma gondii, like all apicomplexan parasites, uses

210 defense against the intracellular pathogens Toxoplasma gondii, Listeria monocytogenes, and Mycobacte

211 nfections with pathogens such as Zika virus, Toxoplasma gondii, Listeria monocytogenes, Treponema pal

212 pathogens, including the protozoan parasite Toxoplasma gondii, live inside a vacuole that resides in

213 nd/or CARD8, including anthrax lethal toxin, Toxoplasma gondii, Shigella flexneri and the small molec

214 iments performed on the rat pineal gland and Toxoplasma gondii, successfully detecting known and prev

215 stigate the ATP4 protein of the apicomplexan Toxoplasma gondii, TgATP4.

216 e function of a large coiled-coil protein in Toxoplasma gondii, TgCep250, in connecting the two centr

217 In apicomplexan parasites such as Toxoplasma gondii, the apical complex includes a spiral

218 In Toxoplasma gondii, the apical complex is a central site

219 The protozoan parasite Toxoplasma gondii, the causative agent of toxoplasmosis,

220 As a major natural host for Toxoplasma gondii, the mouse is widely used for the stud

221 use pathogens, Heligmosomoides polygyrus and Toxoplasma gondii, to investigate the negative impact of

222 complexa phylum, such as Plasmodium spp. and Toxoplasma gondii, undergo complex life cycles involving

223 ed how CD8(+) T cells remove tissue cysts of Toxoplasma gondii, which can grow to the size of >50 mum

224 trol infection by the intracellular parasite Toxoplasma gondii, which corresponded to defects in mono

225 sion pathway analogous to that described for Toxoplasma gondii, with infectious stages traveling in f

226 ded creature can be an intermediate host for Toxoplasma gondii.

227 ogens such as Mycobacterium tuberculosis and Toxoplasma gondii.

228 sential enzyme in the opportunistic pathogen Toxoplasma gondii.

229 vel tool for visualising F-actin dynamics in Toxoplasma gondii.

230 arasitic pathogens Plasmodium falciparum and Toxoplasma gondii.

231 niche for apicomplexan parasites, including Toxoplasma gondii.

232 ium tuberculosis, Pneumocystis jirovecii, or Toxoplasma gondii.

233 cycle of the eukaryotic single-cell parasite Toxoplasma gondii.

234 with the brain-dwelling, protozoan parasite, Toxoplasma gondii.

235 parasitic infections in the world, caused by Toxoplasma gondii.

236 s a disease caused by the protozoan parasite Toxoplasma gondii.

237 pathogens, including the protozoan parasite Toxoplasma gondii.

238 ration of TH1 cells following infection with Toxoplasma gondii.

239 the globally prevalent apicomplexan parasite Toxoplasma gondii.

240 etroviruses, Mycobacterium tuberculosis, and Toxoplasma gondii.

241 nvasion and egress by the protozoan parasite Toxoplasma gondii.

242 Toxoplasma has a multistage life cycle that is intimatel

243 tion-level averages of monocyte responses to Toxoplasma have sometimes produced contradictory results

244 Apicomplexa phylum, including Plasmodium and Toxoplasma, have two types of secretory organelles (micr

245 investigate the roles of specific glycans in Toxoplasma, here we coupled genetic and glycomics approa

246 A new study reveals that Toxoplasma identifies cats based on a single fatty acid,

247 o have had a recent infection with T. gondii Toxoplasma IgA antibody testing can therefore improve th

248 Sabin-Feldman dye test for the detection of Toxoplasma IgG antibodies.

249 aches should include, at least, detection of Toxoplasma IgG, IgM, and IgA and a comprehensive review

250 le-cell RNA-sequencing (scRNA-seq) on >5,400 Toxoplasma in both tachyzoite and bradyzoite stages usin

251 Here we report that Toxoplasma-induced death of human macrophages requires G

252 These findings uncover the Toxoplasma-induced monocyte transcriptional heterogeneit

253 Because latent Toxoplasma infection (LTI) may adversely impact brain fu

254 mechanistic explanation for the link between Toxoplasma infection and psychiatric disorders.

255 d that attraction to predator odor following Toxoplasma infection is not specific to felines.

256 Our findings suggest that chronic Toxoplasma infection leads to cortical neurodegeneration

257 Here we demonstrate that Toxoplasma infection results in increased biogenesis of

258 M21 knockout mice were highly susceptible to Toxoplasma infection, exhibiting decreased levels of ser

259 like many host processes dysregulated during Toxoplasma infection, the induction of lipid droplet gen

260 ological changes in a mouse model of chronic Toxoplasma infection.

261 Current molecular studies on monocyte-Toxoplasma interactions are based on average cell or par

262 a molecular understanding of human monocyte-Toxoplasma interactions can expedite the development of

263 identify open questions in this area of host-Toxoplasma interactions.

264 Toxoplasma is a highly successful parasite that causes l

265 ely, our results describe a unique family of Toxoplasma kinases and implicate phosphorylation of secr

266 essor of Ca(2+)-dependent cell egress during Toxoplasma lytic growth.

267 Its replacement with the I domain from Toxoplasma MIC2 fully restores tissue invasion and paras

268 Toxoplasma multiplies in a membrane-bound parasitophorou

269 We identified the Toxoplasma orthologue of the conserved kinase ERK7 as es

270 ages requires GBP1 and its ability to target Toxoplasma parasitophorous vacuoles through its GTPase a

271 itive recipients unable to take prophylaxis, toxoplasma PCR surveillance should be routinely performe

272 teins, a limitation we recently overcame for Toxoplasma (Periz et al, 2017).

273 This work also identifies a key element of Toxoplasma persistence and suggests that VAC proteolysis

274 based on the serum IgG results: positive for Toxoplasma, positive for cytomegalovirus (CMV), and sero

275 Unlike most eukaryotes, Toxoplasma propagates in intracellular parasitophorous v

276 a major role in determining antigenicity of Toxoplasma proteins.

277 Although it is known that Toxoplasma replicates slowly within intracellular cysts

278 This parasite-driven host defense limits Toxoplasma replication while maintaining host survival,

279 Sangare et al. show that the Toxoplasma retromer complex is essential for parasite vi

280 n human primary fibroblasts, the polymorphic Toxoplasma-secreted effector GRA15 mediates the recruitm

281 Toxoplasma secretes numerous proteins to modify the form

282 We demonstrate that Toxoplasma sequesters a broad range of Rab vesicles into

283 entification, isolation, and analyses of the Toxoplasma serine palmitoyltransferase, an enzyme cataly

284 erformed at the Palo Alto Medical Foundation Toxoplasma Serology Laboratory (PAMF-TSL).

285 The lesions in Toxoplasma serology-positive cases were mostly flat to s

286 Understanding the mechanism of Toxoplasma Skp1 glycosylation is expected to help develo

287 For Toxoplasma species, calcium-dependent protein kinases (C

288 Finally, by showing that a Toxoplasma strain deficient in exporting a specific clas

289 Toxoplasma strain differences in susceptibility to human

290 Here, we discuss how Toxoplasma strain type and parasite effectors influence

291 ly during infection with genetically diverse Toxoplasma strains but also with Neospora caninum, which

292 apical ring, as we show is also the case in Toxoplasma tachyzoites.

293 er proinflammatory cytokines when exposed to toxoplasma tachyzoites.

294 In Toxoplasma, the presence of a contrasting penultimate su

295 are promising late leads for improving anti-Toxoplasma therapy.

296 ed secretion and trafficking systems used by Toxoplasma to overcome the barrier of the parasitophorou

297 be lethal, it is important to understand how Toxoplasma traffics to these tissues, how the immune res

298 Here, we found that Toxoplasma utilizes a cytoplasmic glycosyltransferase fr

299 rives recruitment of TRIM21 to GBP1-positive Toxoplasma vacuoles, leading to Lys63-linked ubiquitinat

300 atial requirements for F-actin regulation in Toxoplasma which appear to be achieved by partially over