ライフサイエンスコーパス: Toxoplasma

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

2 ts of 4-10 genes, depending on the strain of Toxoplasma.

3 ence of a functional heterophagic pathway in Toxoplasma.

4 ryotes and even the closely related parasite Toxoplasma.

5 uced clearance of vacuolar pathogens such as Toxoplasma.

6 t associated with the conoid in apicomplexan Toxoplasma.

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

8 Toxoplasma and Cryptosporidium infect millions of people

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

10 more, we show that TgEB1's MT association in Toxoplasma and in a heterologous system (Xenopus) is bas

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

12 Toxoplasma and Plasmodium mitochondria operate canonical

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

14 gnaling regulates carbohydrate metabolism in Toxoplasma and that the post-translational control of th

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

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

17 rol in a sterol-auxotrophic organism such as Toxoplasma, and furthermore opens up possibilities of ex

18 Hence, Toxoplasma appears to specifically impact levels of circ

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

20 HMA is present in type I and III strains of Toxoplasma but missing in type II strains, both in vitro

21 Toxoplasma gondii, but prior infection with Toxoplasma can inhibit this response.

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

23 ever, IgM can persist for several years, and Toxoplasma commercial IgM diagnostic test kits can yield

24 Similarly, the use of Toxoplasma-Cre parasite strains indicated that dendritic

25 Cre recombinase with their rhoptry proteins (Toxoplasma-Cre) was combined with Ai6 Cre reporter mice

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

27 Protozoan parasites, such as Plasmodium, Toxoplasma, Cryptosporidium, trypanosomes, and Leishmani

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

29 identified machinery required for export of Toxoplasma effectors into the infected host cell.

30 8 exhaustion has been previously reported in Toxoplasma encephalitis (TE)-susceptible model, our curr

31 tumoral injection of an attenuated strain of Toxoplasma gondii (cps) that cannot replicate in vivo an

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

33 oites of the apicomplexan protozoan parasite Toxoplasma gondii (T. gondii).

34 y Pneumocystis jirovecii (P. jirovecii, pj), Toxoplasma gondii (T. gondii, tg), and Mycobacterium avi

35 3 in the parasites of this phylum, including Toxoplasma gondii (TgElp3), possesses a unique C-termina

36 olar proton pyrophosphatase (H(+) -PPase) of Toxoplasma gondii (TgVP1), a membrane proton pump, local

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

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

39 dence of primary gestational infections with Toxoplasma gondii and congenital toxoplasmosis in Austri

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

41 a-mediated elimination of pathogens, such as Toxoplasma gondii and murine norovirus.

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

43 comparative activities of ADF proteins from Toxoplasma gondii and Plasmodium falciparum, the human m

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

45 How the protozoan pathogen Toxoplasma gondii and related parasites shuttle proteins

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

47 Upon infections with Toxoplasma gondii and vaccinia virus, mice with stabiliz

48 Here we tested this model using the Toxoplasma gondii apical membrane protein 1 (TgAMA1), wh

49 Plasmodium falciparum and Toxoplasma gondii are widely studied parasites in phylum

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

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

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

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

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

55 tent and selective inhibitor (compound 1) of Toxoplasma gondii calcium-dependent protein kinase 1 (Tg

56 Reactivation of chronic infection with Toxoplasma gondii can cause life-threatening toxoplasmic

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

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

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

60 at removal of the autoinhibitory domain from Toxoplasma gondii CDPK1 is not sufficient for kinase act

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

62 inst intracellular pathogens, especially for Toxoplasma gondii control.

63 The intracellular parasite Toxoplasma gondii converts from a rapidly replicating ta

64 The obligate intracellular parasite Toxoplasma gondii critically relies on host cell invasio

65 The Toxoplasma gondii cyst stage is resistant to drug therap

66 The protozoan parasite Toxoplasma gondii develops within a parasitophorous vacu

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

68 When Toxoplasma gondii egresses from the host cell, glycerald

69 Toxoplasma gondii encodes three protein kinase A catalyt

70 The genome of Toxoplasma gondii encodes ubiquitination machinery, but

71 The intracellular parasite Toxoplasma gondii enjoys a wide host range and is adept

72 cellular pathogen, the apicomplexan parasite Toxoplasma gondii evades immune system-mediated clearanc

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

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

75 The intracellular parasite Toxoplasma gondii has multiple strategies to alter host

76 A chronic infection with the parasite Toxoplasma gondii has previously been shown to protect m

77 ROP16 is a protein kinase of Toxoplasma gondii identified in the mouse model as a vir

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

79 Using the zoonotic parasite Toxoplasma gondii in California, USA as a model for coas

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

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

82 elements for detection and immune control of Toxoplasma gondii in mice, but not in humans.

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

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

85 intain the latency of chronic infection with Toxoplasma gondii in the brain.

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

87 Chronic infection with Toxoplasma gondii induces a potent resistance against re

88 is essential for CD8+ T-cell recognition of Toxoplasma gondii infected cells.

89 Toxoplasma gondii infection causes substantial morbidity

90 Toxoplasma gondii infection has been described previousl

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

92 n, although their role in protection against Toxoplasma gondii infection is not thoroughly understood

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

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

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

96 rns of hydrocephalus secondary to congenital Toxoplasma gondii infection were identified and characte

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

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

99 immunity exacerbates ileitis induced by oral Toxoplasma gondii infection.

100 osis Study (NCCCTS) have a high incidence of Toxoplasma gondii infection.

101 August 2010 for serologic evidence of recent Toxoplasma gondii infection.

102 into host cells through endocytic pathways, Toxoplasma gondii initiates infection at the cell surfac

103 Toxoplasma gondii is a classic model for studying obliga

104 Toxoplasma gondii is a common parasite of humans and ani

105 Coastal habitat contamination with Toxoplasma gondii is a health risk to humans and marine

106 Toxoplasma gondii is a highly prevalent obligate intrace

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

108 The intracellular protozoan parasite Toxoplasma gondii is a major food-borne illness and oppo

109 Toxoplasma gondii is a protist parasite of warm-blooded

110 Toxoplasma gondii is a protozoan pathogen in the phylum

111 Toxoplasma gondii is a widespread parasite of warm-blood

112 Toxoplasma gondii is a widespread parasitic pathogen tha

113 Toxoplasma gondii is a widespread protozoan parasite inf

114 The obligate intracellular parasite Toxoplasma gondii is able to infect a broad range of hos

115 The obligate intracellular parasite Toxoplasma gondii is able to infect nearly all nucleated

116 Infection with Toxoplasma gondii is acquired through consumption of und

117 Toxoplasma gondii is among the most prevalent parasites

118 Toxoplasma gondii is an apicomplexan parasite that cause

119 The parasite Toxoplasma gondii is an environmentally persistent patho

120 Toxoplasma gondii is an intracellular parasite that caus

121 Toxoplasma gondii is an obligate intracellular parasite

122 Toxoplasma gondii is an obligate intracellular parasite

123 Toxoplasma gondii is an obligate intracellular parasite

124 Toxoplasma gondii is an obligate intracellular parasite

125 Toxoplasma gondii is an obligate intracellular protozoan

126 Toxoplasma gondii is an obligate, intracellular eukaryot

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

128 Cerebral infection with the parasite Toxoplasma gondii is followed by activation of resident

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

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

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

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

133 Infection by Toxoplasma gondii leads to massive changes to the host c

134 he founding member of the class XIVa family, Toxoplasma gondii myosin A (TgMyoA), is a monomeric unco

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

136 Toxoplasma gondii parasites must actively invade host ce

137 Bradyzoite forms of Toxoplasma gondii persist in tissue cysts for the lifeti

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

139 Toxoplasma gondii replicates asexually by a unique inter

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

141 mucosal responses to the protozoan parasite Toxoplasma gondii resulted in dysbiosis and the eliminat

142 ted in a 100% reduction in the recurrence of Toxoplasma gondii retinochoroiditis over 1 year of treat

143 from Campinas, Brazil, with active recurrent Toxoplasma gondii retinochoroiditis were included.

144 A recent study in Toxoplasma gondii revealed a unique bipartite structure

145 The reduction in invasiveness of the Toxoplasma gondii RH-AMA1 knockout (RH-AMA1(KO)) tachyzo

146 Transmissible stages of Toxoplasma gondii store energy in the form of the carboh

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

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

149 d that systemic infection with the protozoan Toxoplasma gondii triggers not only a transient increase

150 e to reactivation of cerebral infection with Toxoplasma gondii using a murine model.

151 pes 1 and 2, Mycobacterium tuberculosis, and Toxoplasma gondii via real-time polymerase chain reactio

152 The Toxoplasma gondii virulence factors ROP5 and ROP18 both

153 Toxoplasma gondii was not detected in field-collected sn

154 ng pathways that regulate these processes in Toxoplasma gondii We found that microneme secretion was

155 Salmonella typhimurium or Toxoplasma gondii were administered to knockout (KO) mic

156 ded in apicomplexan parasites, especially in Toxoplasma gondii where 14 separate genes encoding these

157 The survival of Toxoplasma gondii within its host cell requires protein

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

159 Intriguingly, Toxoplasma gondii, a highly successful apicomplexan para

160 in CNS infections, including infection with Toxoplasma gondii, a protozoan parasite that naturally e

161 Toxoplasma gondii, an apicomplexan parasite prevalent in

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

163 Toxoplasma gondii, an obligate intracellular protozoan p

164 morbillivirus, herpesvirus, West Nile virus, Toxoplasma gondii, and Brucella spp.

165 Th17 cell responses to herpes simplex virus, Toxoplasma gondii, and Citrobacter rodentium infections.

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

167 esistance against a prototypic Th1 pathogen, Toxoplasma gondii, and for the generation of pathogen-sp

168 c cells (DCs) are critical for resistance to Toxoplasma gondii, and infection with this pathogen lead

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

170 After acute oral infection with Toxoplasma gondii, both WT and Crtam(-/-) mice mounted a

171 t defense against the intracellular pathogen Toxoplasma gondii, but prior infection with Toxoplasma c

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

173 In Toxoplasma gondii, disruption of the first, fifth, or si

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

175 In Toxoplasma gondii, extracellular potassium levels and ot

176 In Toxoplasma gondii, fatty acid synthesis via the apicopla

177 gMyoA, a class XIVa myosin from the parasite Toxoplasma gondii, is required for the parasite to effic

178 Toxoplasma gondii, like all apicomplexan parasites, uses

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

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

181 , including Bacillus anthracis lethal toxin, Toxoplasma gondii, muramyl dipeptide, and host intracell

182 ed to functions within pathways/networks for Toxoplasma gondii, Neospora caninum, Cryptosporidium and

183 Indeed, in mice challenged with the parasite Toxoplasma gondii, NK and T cell responses are character

184 medical and veterinary importance, including Toxoplasma gondii, Plasmodium falciparum, and C. parvum

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

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

187 Toxoplasma gondii, the causative agent of toxoplasmosis,

188 Toxoplasma gondii, the causative agent of toxoplasmosis,

189 Toxoplasma gondii, the most common parasitic infection o

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

191 In the ubiquitous protozoan parasite Toxoplasma gondii, the oocyst stage possesses a bilayere

192 use pathogens, Heligsomosoides polygyrus and Toxoplasma gondii, to investigate the negative impact of

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

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

195 ne the polymerization properties of actin in Toxoplasma gondii, unexpectedly finding that it exhibits

196 pathogens, including the protozoan parasite Toxoplasma gondii.

197 ration of TH1 cells following infection with Toxoplasma gondii.

198 sential enzyme in the opportunistic pathogen Toxoplasma gondii.

199 or the lytic cycle of the protozoan parasite Toxoplasma gondii.

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

201 long immunity to virulent acute infection by Toxoplasma gondii.

202 omposition and function in the centrosome of Toxoplasma gondii.

203 a parasite Plasmodium falciparum and related Toxoplasma gondii.

204 obligate intracellular apicomplexan parasite Toxoplasma gondii.

205 es (ROPs) are essential virulence factors of Toxoplasma gondii.

206 onmentally driven infectious disease such as Toxoplasma gondii.

207 autophagy related 5 (Atg5) in resistance to Toxoplasma gondii.

208 s gliding motility and host cell invasion by Toxoplasma gondii.

209 es of this cytokine following challenge with Toxoplasma gondii.

210 the immune system responds to infection with Toxoplasma gondii.

211 (ROP5) expressed by the protozoan parasite, Toxoplasma gondii.

212 we identified candidates for APT activity in Toxoplasma gondii.

213 arasitic pathogens Plasmodium falciparum and Toxoplasma gondii.

214 niche for apicomplexan parasites, including Toxoplasma gondii.

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

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

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

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

219 r of pathogens (CMV, candida, mycobacterium, toxoplasma, HIV, p < 0.04 in all cases), compared to Uto

220 ly of the first three sugars is dependent on Toxoplasma homologs of Gnt1 and PgtA.

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

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

223 For Toxoplasma IgM and IgA antibodies, there is no reference

224 test results for 451 patients with positive Toxoplasma IgM and IgG test results obtained at nonrefer

225 Positive Toxoplasma IgM and IgG test results obtained at NRLs can

226 A positive Toxoplasma immunoglobulin M (IgM) result is often interp

227 housands of the transcriptional changes that Toxoplasma imparts on its host cell.

228 d macrophage (BMDM) inflammasome response to Toxoplasma independent of the lethal factor proteolysis

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

230 Here we show that Toxoplasma infection actives an inflammasome response in

231 compromised state that both promotes chronic toxoplasma infection and leads to decreased resistance t

232 oxoplasmosis Register of pregnant women with Toxoplasma infection and their offspring with births bet

233 For these reasons, a chronic Toxoplasma infection can be erroneously classified as an

234 Annually, 8.5 per 10 000 women acquired Toxoplasma infection during pregnancy, and 1.0 per 10 00

235 Toxoplasma infection is sufficient to generate an inflam

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

237 results highlight the ability of intestinal Toxoplasma infection to alter mucosal DC activity at bot

238 as administered to women from diagnosis of a Toxoplasma infection until delivery.

239 te that NLRP1 is an innate immune sensor for Toxoplasma infection, activated via a novel mechanism th

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

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

242 included 2147 pregnant women with suspected Toxoplasma infection.

243 nown to date, is not observed in response to Toxoplasma infection.

244 This secreted effector, toxoplasma inhibitor of STAT1-dependent transcription (T

245 nfection with a type I, II, or III strain of Toxoplasma inhibits the dissociation of STAT1 from DNA,

246 We report here that a type I strain of Toxoplasma inhibits the expression of primary IFN-gamma

247 sponsible for controlling development in the Toxoplasma intermediate life cycle have long been sought

248 Resistance to Toxoplasma is dependent on gamma interferon (IFN-gamma)

249 Acute infection by Toxoplasma is hallmarked by rapid proliferation in its h

250 t protozoan parasites such as Plasmodium and Toxoplasma, is poorly understood.

251 By exploiting a mutant of Toxoplasma lacking the cathepsin protease L, Dou et al.

252 naturally occurring HMA+ and HMA- strains of Toxoplasma, Legionella, and Chlamydia indicates the exis

253 iguingly, several infectious agents, such as Toxoplasma, Legionella, and Chlamydia, have been reporte

254 The protozoan parasite, Toxoplasma, like many intracellular pathogens, suppresse

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

256 When infected with toxoplasma, mice that selectively lack GC receptor (GR)

257 Toxoplasma multiplies in a membrane-bound parasitophorou

258 Toxoplasma NR and Type II serotypes predominate in Germa

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

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

261 a major role in determining antigenicity of Toxoplasma proteins.

262 sis sent to the Palo Alto Medical Foundation Toxoplasma Reference Laboratory from June 2004 through A

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

264 In mammalian cells, the protozoan pathogen Toxoplasma resides in a nonfusiogenic vacuole that segre

265 ficient mice with the intracellular parasite Toxoplasma results in impaired production of the STAT1-d

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

267 We obtained the Toxoplasma ROP16 locus DNA sequence in samples from 12 p

268 ms, and policy makers to consider preventive Toxoplasma screening as a potential tool to reduce the i

269 We have identified GRA17 as a Toxoplasma-secreted protein that localizes to the parasi

270 Toxoplasma secretes numerous proteins to modify the form

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

272 threonine residues that are targeted by the Toxoplasma Ser/Thr kinases, ROP17 and ROP18.

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

274 Interpretation of Toxoplasma serology at a reference laboratory can help d

275 ere referred to Palo Alto Medical Foundation Toxoplasma Serology Laboratory (PAMF-TSL) to determine w

276 vant clinical characteristics, the recipient Toxoplasma serostatus was not associated with mortality

277 variate analysis, however, showed that donor Toxoplasma serostatus was not independently associated w

278 Toxoplasma serotypes in consecutive serum samples from G

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

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

281 genetic crosses between type II and type III Toxoplasma strains and quantitative trait locus (QTL) ma

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

283 g improved genetic models based on Deltaku80 Toxoplasma strains will stimulate development of highly

284 rt chains, although the roles differ between Toxoplasma tachyzoites and Plasmodium erythrocytic stage

285 able to survive an otherwise lethal dose of Toxoplasma tachyzoites and that complementation of the m

286 ids, while in Plasmodium liver stages and in Toxoplasma tachyzoites fatty acid synthesis is an essent

287 hondria may represent a novel means by which Toxoplasma tachyzoites manipulate the host.

288 er proinflammatory cytokines when exposed to toxoplasma tachyzoites.

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

290 in LTI patients with NCI and trials of anti-Toxoplasma therapy should be pursued.

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

292 Oral infection with Toxoplasma triggers an inflammasome response that is pro

293 ent uracil auxotroph vaccine strain (cps) of Toxoplasma triggers novel innate immune responses that s

294 Toxoplasma type I infection also inhibits IFN-beta-induc

295 Recently, it was reported that the Toxoplasma type II NTE strain prevents the recruitment o

296 Apicomplexa parasite genera, Plasmodium and Toxoplasma, until we genetically engineered viable paras

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

298 Using a Toxoplasma vaccination model, we delineate the sequence

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

300 ins into the host cell by a type I strain of Toxoplasma without complete parasite invasion is not suf