ライフサイエンスコーパス: gondii

1 ant target of inhibition of resistance in T. gondii.

2 e can be an intermediate host for Toxoplasma gondii.

3 as Mycobacterium tuberculosis and Toxoplasma gondii.

4 idative stress as a mechanism for killing T. gondii.

5 PKA and PKG pathways to govern egress in T. gondii.

6 yme in the opportunistic pathogen Toxoplasma gondii.

7 r visualising F-actin dynamics in Toxoplasma gondii.

8 thogens Plasmodium falciparum and Toxoplasma gondii.

9 apicomplexan parasites, including Toxoplasma gondii.

10 losis, Pneumocystis jirovecii, or Toxoplasma gondii.

11 e immune status of animals/humans against T. gondii.

12 y prevalent apicomplexan parasite Toxoplasma gondii.

13 o only those patients recently exposed to T. gondii.

14 , Mycobacterium tuberculosis, and Toxoplasma gondii.

15 egress by the protozoan parasite Toxoplasma gondii.

16 with the intracellular protozoan Toxoplasma gondii(1).

17 how immunity is elicited against Toxoplasma gondii - a complex pathogen with multiple mechanisms of

18 Toxoplasma gondii, a common neurotropic parasite, is increasingly b

19 een the lytic and latent forms of Toxoplasma gondii, a parasite that causes a persistent brain infect

20 Toxoplasma gondii, a protozoan parasite, undergoes a complex and po

21 ge of the genetic tractability of Toxoplasma gondii, a related parasite that shows moderate sensitivi

22 of the dpy19 gene in the parasite Toxoplasma gondii abolished C-mannosyltransferase activity and redu

23 ted H4K31 is enriched in the core body of T. gondii active genes but inversely correlates with transc

24 agy in CD40(+) endothelial cells and anti-T. gondii activity dependent on ULK1 and beclin 1.

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

26 cryotrapped in the active site of Toxoplasma gondii aldolase crystals to high resolution.

27 Toxoplasma gondii, an obligate intracellular protozoan parasite, es

28 erates during gliding motility in Toxoplasma gondii and appears to be crucial for the establishment o

29 ional reverse transsulfuration pathway in T. gondii and demonstrates the crucial role of TgCBS in bio

30 innate immune responses to N. caninum and T. gondii and found marked differences in cytokine levels a

31 previously undescribed apical proteins in T. gondii and identify an essential component named conoid

32 chanism of inhibition of TLR signaling by T. gondii and IL-10 and suggest potential negative conseque

33 maging flow cytometry, we found that both T. gondii and IL-10 inhibited virus-induced nuclear translo

34 actinonin in the related parasite Toxoplasma gondii and implicated P. falciparum FtsH1 as a likely ta

35 Clusters of T. gondii and individual monocytes across the brain were id

36 coplast has a key role in heme biology in T. gondii and is important for both mitochondrial and gener

37 odium species that cause malaria, Toxoplasma gondii and kinetoplastid protozoa, including Trypanosoma

38 th the common coccidian parasites Toxoplasma gondii and Neospora caninum activated GABAergic signalin

39 se associated with emerging haplotypes of T. gondii and our lack of effective treatments to sterilize

40 rimarily focuses on studies using Toxoplasma gondii and Plasmodium spp. as the best studied apicomple

41 Apicomplexan parasites Toxoplasma gondii and Plasmodium spp. use latent stages to persist

42 Using Toxoplasma gondii and Salmonella enterica Typhimurium we demonstrat

43 The apical complex of Toxoplasma gondii and some other apicomplexans includes a cone-shap

44 tment of the autophagy protein LC3 around T. gondii and spontaneous parasite killing dependent on the

45 7 knockout mice were infected orally with T. gondii and their pathologic profiles were analyzed.

46 lated evidence on the associations between T.gondii and various human neuropsychiatric disorders and

47 al pathogens (West Nile virus and Toxoplasma gondii) and one with Streptococcus species with other ba

48 hat contributes to resistance to invading T. gondii, and they thus unveil new avenues for developing

49 that seroprevalence of Brucella spp. and T. gondii antibodies likely increased through time, and pro

50 levated levels of anti-Toxoplasma gondii (T. gondii) antibodies in patients with major mental illness

51 e/Phe genotype was associated with higher T. gondii antibody levels in sera.

52 Natural and engineered T. gondii antigens have led the way to understanding the fa

53 icroscopy (U-ExM) to localize the Toxoplasma gondii Apical Cap protein 9 (AC9) and its partner AC10,

54 caused by the protozoan parasite Toxoplasma gondii are poorly understood.

55 identify cats as the definitive host for T. gondii are unknown.

56 ent in immunodeficient mice infected with T. gondii, as associated with high expression level (P <= 0

57 Here we establish that Toxoplasma gondii aspartyl protease 3 (ASP3) resides in the endosom

58 d as acutely or chronically infected with T. gondii based on a panel of serologic tests performed at

59 still major holes in our understanding of T. gondii biology, including the genes controlling parasite

60 deum, and the protozoan parasite, Toxoplasma gondii, both lacking HIF.

61 nzyme B were detected in association with T. gondii bradyzoites.

62 we show that IL-1R(-/-) mice can control T. gondii burden throughout infection.

63 the motility apparatus of living Toxoplasma gondii by adhering a microsphere to the surface of an im

64 11 induced a potent chemokine response to T. gondii by engaging its receptor RAGE, and regulated mono

65 r experiments reveal a sensing system for T. gondii by human cells that is based on the detection of

66 e intracellular vacuolar pathogen Toxoplasma gondii by inducing the destruction of the parasitophorou

67 rvention to combat chronic infection with T. gondii by targeting the persistent cysts of the parasite

68 In summary, our results indicate that T. gondii C-mannosyltransferase DPY19 is not essential for

69 shown to be potent inhibitors of Toxoplasma gondii calcium-dependent protein kinase 1.

70 ng cat litter, as maternal infection with T. gondii can be transmitted to the fetus with potentially

71 l cycle of the protistan parasite Toxoplasma gondii can occur in any warm-blooded mammal, the sexual

72 The apicomplexan parasite Toxoplasma gondii causes macrophage death through unidentified mech

73 pyrazolopyrimidine inhibitors of Toxoplasma gondii CDPK1 demonstrated in vitro and in vivo efficacy.

74 have recently reported that the putative T. gondii CGL gene encodes a functional enzyme.

75 As T. gondii chronic infection and profilin (PRF) confer resis

76 Toxoplasma gondii chronically infects a quarter of the world's popu

77 T. gondii circulates in the bloodstream within infected leu

78 be significantly correlated with sites of T. gondii clusters.

79 lization of monocytes in the brain during T. gondii CNS infection.

80 ction, the intracellular parasite Toxoplasma gondii co-opts critical functions of its host cell to av

81 due to varicella-zoster virus and Toxoplasma gondii coinfection documented by polymerase chain reacti

82 ary to varicella-zoster virus and Toxoplasma gondii coinfection in a male patient in Bogota, Colombia

83 st potential negative consequences of HIV/T. gondii coinfection.

84 one-shaped assembly, the conoid, which in T. gondii comprises 14 spirally arranged fibers that are no

85 Toxoplasma gondii contains a limited subset of actin binding protei

86 e to the pathogens Brucella spp., Toxoplasma gondii, Coxiella burnetii, Francisella tularensis, and N

87 mechanism that functions against not only T. gondii cysts but also other large targets, including sol

88 .2 chain have a potent activity to remove T. gondii cysts from the brain.

89 T cells to penetrate into a large target, T. gondii cysts, for their elimination.

90 tivate CD8(+) T cells capable of removing T. gondii cysts.

91 T. gondii Deltagra12 mutants were more vulnerable to be eli

92 retion following infection with wild-type T. gondii, demonstrating that this mutant is an attenuated,

93 partially reversed by a deficiency in the T. gondii-derived ROP16 kinase, known to directly phosphory

94 HC class II tetramer reagent specific for T. gondii did not recognize Tregs isolated from the CNS.

95 Toxoplasma gondii DNA detection is essential to antenatally diagnos

96 ent proteins or targeted genes of Toxoplasma gondii, driven by N. caninum promoters, have yielded rob

97 particular emphasis is placed on Toxoplasma gondii, during both its acute and latent stages of infec

98 a(2+) signaling pathway dictating Toxoplasma gondii egress have been identified, whether the parasite

99 When Toxoplasma gondii egresses from the host cell, glyceraldehyde-3-pho

100 immunoglobulin G (IgG) antibodies against T. gondii embryogenesis-related protein (TgERP).

101 Toxoplasma gondii encodes three protein kinase A catalytic (PKAc1-3

102 To test if these T. gondii experienced NK cells were intrinsically different

103 ual development, this work will allow the T. gondii field to use of alternative models in future stud

104 omeric virulence genes, while the Toxoplasma gondii genome was dominated by clustering of the centrom

105 etic phosphoglycan portion of the Toxoplasma gondii glycosylphosphatidylinositol (GPI1) for the detec

106 opic expression of N. caninum profilin in T. gondii had no impact on early IFN-gamma production or pa

107 icomplexan parasites, loss of TgPOFUT2 in T. gondii had only a modest impact on MIC2 levels and the w

108 Toxoplasma gondii has been taken as an example for this strategy.

109 itionally, the protozoan parasite Toxoplasma gondii has been thought of as relevant to public health

110 e obligate intracellular parasite Toxoplasma gondii has unusually stable cortical microtubules beneat

111 (MIC2), a motility-associated adhesin of T. gondii, has highly glycosylated thrombospondin repeat (T

112 Apicomplexan parasites like Toxoplasma gondii have a specialized cilium-like structure called t

113 Remarkably, at least 350 host species of T. gondii have been described to date, and it is estimated

114 the involvement of the apicoplast in the T. gondii heme biosynthesis pathway, we investigated the ro

115 otein is also thought to be important for T. gondii-host interaction, pathogenesis, and immune evasio

116 ammation and are critical for controlling T. gondii However, the dynamic and regional relationship be

117 ii IgG antibody test results who also had T. gondii IgA and IgM antibody tests performed.

118 ults demonstrate that pregnant women with T. gondii IgA antibodies are more likely than pregnant wome

119 e more likely than pregnant women without T. gondii IgA antibodies to have had a recent infection wit

120 Among the 81 women who were positive by T. gondii IgA antibody ELISA testing, 61 (75.3%) were acute

121 ated the usefulness of adding the Toxoplasma gondii IgA antibody enzyme-linked immunosorbent assay (E

122 Physicians who ordered testing only for T. gondii IgG and IgM should also request additional testin

123 consecutive pregnant women with positive T. gondii IgG antibody test results who also had T. gondii

124 cally disordered component of the Toxoplasma gondii IMC, as essential for apical complex development,

125 higher number of intense bands on aqueous T. gondii immunoblot (P = .006), and increased when venous

126 mer coefficient (GWC), Toxoplasma gondii (T. gondii) immunoblot, or T. gondii-specific polymerase cha

127 N-glycomics changes during infection with T. gondii in BALB/c mice, immunocompetent, or in severe com

128 Nevertheless, atypical strains of T. gondii in endemic locations cause severe pathology in he

129 e strong immune responses against Toxoplasma gondii in HLA supermotif, transgenic mice.

130 The importance of T. gondii in human health was made clear with the first rep

131 abundant (P <= 0.001 each), during acute T. gondii in immunocompetent mice, compared to controls.

132 Brain infection by the parasite Toxoplasma gondii in mice is thought to generate vulnerability to p

133 ontributes to the virulence and growth of T. gondii in mice.

134 ntify NLRP3 as an inflammasome sensor for T. gondii in primary human peripheral blood cells and to de

135 mechanisms of cell-intrinsic immunity to T. gondii in the brain and muscle, and the long-term effect

136 screens in Plasmodium berghei and Toxoplasma gondii, in which pooled transfections of multiple vector

137 to the intracellular replicative cycle of T. gondii including secretion of adhesins, motility, invasi

138 Here, the longevity of the T. gondii-induced chronic cachexia model revealed that cach

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

140 We have recently shown that T. gondii-induced muscle atrophy meets the clinical definit

141 T. gondii induces EGFR signaling in vitro during invasion o

142 Optical clearing of intact T. gondii-infected brains using iDISCO(+) and light-sheet m

143 Circulating T. gondii-infected leukocytes (dendritic cells used as a mo

144 as significantly lower or undetectable in T. gondii-infected mice during the first 24 hpi.

145 ress of anhedonia and despair symptoms of T. gondii-infected subjects.

146 Here we report that during T. gondii infection a strong NF-kappaB and inflammatory cyt

147 ver, a novel biomarker that correlated to T. gondii infection and associated behaviors is demanded.

148 erstanding of the host immune response to T. gondii infection and summarize the key limitations for t

149 s differentially expressed in response to T. gondii infection are similar between males and females.

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

151 uman monocytes recognized the presence of T. gondii infection by detecting the alarmin S100A11 protei

152 lammation generated by certain strains of T. gondii infection can be neuroprotective in the context o

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

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

155 However, latent T.gondii infection has been increasingly associated with a

156 Toxoplasma gondii infection in mice provides an excellent model for

157 The course of Toxoplasma gondii infection in rats closely resembles that in human

158 Toxoplasma gondii infection is an asymptomatic disease, with lethal

159 However, the role of the IL-1 axis in T. gondii infection is unclear.

160 elop these characteristics during Toxoplasma gondii infection is unknown.

161 We argue that the occult effects of latent T.gondii infection likely outweigh the recognised overt mo

162 monocytes into the blood and brain during T. gondii infection of C57BL/6J and CCR2(RFP/+)CX3CR1(GFP/+

163 T. gondii infection of resistant and sensitive mouse strain

164 mic and transcriptomic effects of Toxoplasma gondii infection on human host cells and demonstrate tha

165 s both in vitro and in a model of Toxoplasma gondii infection revealed de novo chromatin accessibilit

166 We discuss how T. gondii infection suppresses noradrenergic signaling and

167 ective role for NK cells during secondary T. gondii infection that is dependent on IL-12 and IL-23.

168 t pattern of monocyte infiltration during T. gondii infection to the olfactory tubercle, in contrast

169 gress toward understanding the biology of T. gondii infection using rodent models, human cell experim

170 of GRA12 to the molecular pathogenesis of T. gondii infection were examined in vitro and in vivo.

171 blood-brain barrier (BBB) within 2 wk of T. gondii infection, exhibited distinct rolling and crawlin

172 EW rat versus the BN rat, with or without T. gondii infection, in order to unravel molecular factors

173 cell IFN-gamma production during primary T. gondii infection, in the absence of IL-12 using IL-12p35

174 After T. gondii infection, mice that expressed CD40 restricted to

175 opagate inflammation, and that in chronic T. gondii infection, microglia can release the alarmin IL-1

176 s related to the establishment of Toxoplasma gondii infection, such as the formation of the intravacu

177 1beta cleavage and release in response to T. gondii infection, without affecting the release of TNF-a

178 using a vaccine-challenge mouse model of T. gondii infection.

179 involved in host immune responses against T. gondii infection.

180 ell responses in the brain during chronic T. gondii infection.

181 r control of and survival after secondary T. gondii infection.

182 topathology in the brain and retina after T. gondii infection.

183 te responses and pathology during Toxoplasma gondii infection.

184 and was not induced in macrophages during T. gondii infection.

185 ons regulates their local behavior during T. gondii infection.

186 ), modifies gene expression patterns upon T. gondii infection.

187 and parasite, that facilitate persistent T. gondii infection.

188 he most common method to diagnose Toxoplasma gondii infections is the serological determination of an

189 pensable in T. gondii tachyzoites and for T. gondii infectivity.

190 The intracellular parasite Toxoplasma gondii infects nucleated cells in virtually all warm-blo

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

192 The Toxoplasma gondii inner membrane complex (IMC) is an important orga

193 uorescence microscopy, we determined that T. gondii invaded but did not induce IFN-alpha or TNF-alpha

194 ell-leukocyte interaction, CD40 restricts T. gondii invasion of neural tissue through a mechanism tha

195 Altogether, EGFR is a novel regulator of T. gondii invasion of neural tissue, enhancing invasion lik

196 fects of endothelial cell CD40 on Toxoplasma gondii invasion of the retina and brain, organs seeded h

197 Toxoplasma gondii is a common protozoan parasite that infects up to

198 f HIV type 1 replication, whereas Toxoplasma gondii is a life-threatening opportunistic infection in

199 ction with the protozoan parasite Toxoplasma gondii is a major health risk owing to birth defects, it

200 Toxoplasma gondii is a remarkably successful protozoan parasite tha

201 Toxoplasma gondii is a ubiquitous, obligate intracellular eukaryoti

202 Toxoplasma gondii is a widespread parasite with considerable versat

203 The propagation of Toxoplasma gondii is accomplished by repeated lytic cycles of paras

204 Toxoplasma gondii is an incredibly successful parasite owing in par

205 Toxoplasma gondii is an intracellular parasite that causes dissemin

206 Toxoplasma gondii is an intracellular parasite that is highly preva

207 Toxoplasma gondii is an obligate intracellular parasite that establ

208 Toxoplasma gondii is an obligate intracellular parasite that establ

209 Toxoplasma gondii is an obligate protozoan parasite that naturally

210 Toxoplasma gondii is an obligate, intracellular eukaryotic apicompl

211 Toxoplasma gondii is an opportunistic infection that can cause seve

212 Toxoplasma gondii is associated with physiological and psychiatric

213 Toxoplasma gondii is associated with physiological effects in the h

214 Our data indicate that T. gondii is capable of evading host detection during the f

215 of actinonin in P. falciparum and Toxoplasma gondii is FtsH1, a homolog of a bacterial membrane AAA+

216 ts animal counterparts, Skp1 from Toxoplasma gondii is hydroxylated by an O2-dependent prolyl-4-hydro

217 The protozoan parasite Toxoplasma gondii is thought to exploit monocyte trafficking to fac

218 Toxoplasma gondii (T. gondii) is a protozoan parasite that uses conserved mech

219 9 qPCR does not depend on the genotype of T. gondii isolates and that, in fact, it is superior to B1

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

221 Toxoplasma gondii, like all apicomplexan parasites, uses Ca(2+) sig

222 ith pathogens such as Zika virus, Toxoplasma gondii, Listeria monocytogenes, Treponema pallidium, par

223 including the protozoan parasite Toxoplasma gondii, live inside a vacuole that resides in the host c

224 The protozoan parasite Toxoplasma gondii lives inside a vacuole in the host cytosol where

225 Collectively, these data indicate that T. gondii may not cause a life-long CNS infection.

226 othesized that a prolonged infection with T. gondii may protect against age-associated decline in cog

227 cale metabolic model (GEM) of the Toxoplasma gondii metabolic network that incorporates genetic, tran

228 analysis, we found that the four TSRs in T. gondii MIC2 with protein O-fucosyltransferase 2 (POFUT2)

229 mily, is a secreted protein important for T. gondii motility, host cell attachment, invasion, and egr

230 IFN-gamma was partially dependent on the T. gondii mouse profilin receptor Toll-like receptor 11 (TL

231 However, sexual reproduction of T. gondii occurs only in felids, wherein fertilisation of h

232 Horizontal transmission of Toxoplasma gondii occurs primarily via ingestion of environmental o

233 vestigated the impact of coinfection with T. gondii on the innate virus-directed responses of human p

234 fy an intrinsic role for autophagy in the T. gondii parasite and its close relatives.

235 Toxoplasma gondii parasites rapidly exit their host cell when expos

236 of therapeutics that prevent shedding of T. gondii parasites.

237 osteroid administration, aqueous GWC, and T. gondii PCR did not influence recurrences (P = .12, P = .

238 Apicomplexan parasites such as Toxoplasma gondii possess an unusual heme biosynthesis pathway whos

239 Toxoplasma gondii possesses a limited set of actin-regulatory prote

240 The intracellular parasite Toxoplasma gondii possesses three distinct Drps.

241 and colleagues uncover a new role for the T. gondii protein GRA15 in inducing an anti-parasite respon

242 We further demonstrated that the secreted T. gondii protein kinase ROP17 was required for enhanced ti

243 The Toxoplasma gondii PV is filled with a network of tubulated membrane

244 Toxoplasma gondii reaches the CNS by circulating in blood within le

245 Apicomplexan parasites such as Toxoplasma gondii rely on a unique form of locomotion known as glid

246 e obligate intracellular parasite Toxoplasma gondii replicates in an unusual process, described as in

247 e obligate intracellular parasite Toxoplasma gondii reprograms its metabolism.

248 c CNS infection with the parasite Toxoplasma gondii requires ongoing T cell responses in the brain.

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

250 a previously unknown modulator of Toxoplasma gondii resistance in vivo thereby extending host innate

251 e demonstrated that N. caninum expressing T. gondii's GRA15 and ROP16 kinase are biologically active

252 bination with SAG1 may strengthen Toxoplasma gondii serology, in particular in seroepidemiological st

253 the mechanism of species specificity for T. gondii sexual development and break the species barrier

254 of their diet with linoleic acid allowed T. gondii sexual development in mice.

255 We determined that T. gondii sexual development occurs when cultured feline in

256 nt reliance on companion animals to study T. gondii sexual development, this work will allow the T. g

257 s that create a conducive environment for T. gondii sexual reproduction will allow for development of

258 , including anthrax lethal toxin, Toxoplasma gondii, Shigella flexneri and the small molecule DPP8/9

259 Monoclonal T. gondii-specific CD8 T cells adoptively transferred into

260 oplasma gondii (T. gondii) immunoblot, or T. gondii-specific polymerase chain reaction (PCR) in aqueo

261 CRISPR/Cas9 strategy was used to create a T. gondii strain that exhibits defective fertilisation, dec

262 r of two genetically distinct, persistent T. gondii strains (Prugniaud/type II/haplogroup 2 and CEP/t

263 ion of GRA12 in type I RH and type II Pru T. gondii strains did not affect the parasite growth and re

264 immunological phenotypes consistent with T. gondii strains.

265 reported elevated levels of anti-Toxoplasma gondii (T. gondii) antibodies in patients with major men

266 oldmann-Witmer coefficient (GWC), Toxoplasma gondii (T. gondii) immunoblot, or T. gondii-specific pol

267 Toxoplasma gondii (T. gondii) is a protozoan parasite that uses con

268 dings in another study, is dispensable in T. gondii tachyzoites and for T. gondii infectivity.

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

270 ected with the protozoan parasite Toxoplasma gondii (Tg).

271 ATP4 protein of the apicomplexan Toxoplasma gondii, TgATP4.

272 ally characterized cDNA encoding CBS from T. gondii (TgCBS), which represents a first example of prot

273 of a large coiled-coil protein in Toxoplasma gondii, TgCep250, in connecting the two centrosomal core

274 ba Dictyostelium and the parasite Toxoplasma gondii The full effect of hydroxylation requires modific

275 Dictyostelium (a social amoeba), Toxoplasma gondii (the agent for human toxoplasmosis), and other pr

276 In apicomplexan parasites such as Toxoplasma gondii, the apical complex includes a spiral cap of tubu

277 In Toxoplasma gondii, the apical complex is a central site of converge

278 oth result in increased susceptibility to T. gondii, the basis for this phenotype reveals distinct ro

279 The protozoan parasite Toxoplasma gondii, the causative agent of toxoplasmosis, includes b

280 ity primarily facilitate the transport of T. gondii through tissues and promote systemic disseminatio

281 PR screens recently developed for Toxoplasma gondii to discover sensitizing and desensitizing mutatio

282 critical for the transmission of Toxoplasma gondii to the definitive feline host via predation, and

283 odies to have had a recent infection with T. gondii Toxoplasma IgA antibody testing can therefore imp

284 ular proteins, the human pathogen Toxoplasma gondii transfers a different sugar, fucose, to proteins

285 gy could be a useful tool for delineating T. gondii transmission routes in human populations.

286 elative importance of different routes of T. gondii transmission.

287 It is believed that infection by Toxoplasma gondii triggers a lifelong protective immunity due to th

288 RNA-Seq analysis of cat enteric stages of T. gondii uncovered genes expressed uniquely in microgamete

289 ylum, such as Plasmodium spp. and Toxoplasma gondii, undergo complex life cycles involving multiple s

290 ibe the myristoylated proteome of Toxoplasma gondii using chemoproteomic methods and show that a smal

291 trinsic memory-like characteristics after T. gondii vaccination.

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

293 Resistant populations of T. gondii were selected by culture in increasing concentrat

294 +) T cells remove tissue cysts of Toxoplasma gondii, which can grow to the size of >50 mum in diamete

295 ion by the intracellular parasite Toxoplasma gondii, which corresponded to defects in monocyte recrui

296 n was inhibited only in cells infected by T. gondii, which inhibited neither uptake of GFP-HSV nor lo

297 ded to the intracellular parasite Toxoplasma gondii While the loss of IL-27p28 and its overexpression

298 ng, 61 (75.3%) were acutely infected with T. gondii, while of the 547 who were negative by IgA testin

299 y analogous to that described for Toxoplasma gondii, with infectious stages traveling in freshwater r

300 the signals governing the lytic cycle of T. gondii, with particular focus on egress from infected ce