2011
DOI: 10.3923/jp.2011.60.73
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Toxoplasma gondii Strategy for Intracellular Survival: Is it Still Enigmatic?

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Cited by 3 publications
(3 citation statements)
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“…Control Toxo factor-beta) through the differentiation of M2 phenotype macrophages [13,[23][24][25]. The evasion of anti-parasitic effector mechanisms as mediators of the inflammatory response by T. gondii may be induced by brain ischemic tolerance [26]. The HIF family as master regulatory transcription factors upregulate multiple genes controlling neovascularization [27].…”
Section: Control Toxomentioning
confidence: 99%
See 1 more Smart Citation
“…Control Toxo factor-beta) through the differentiation of M2 phenotype macrophages [13,[23][24][25]. The evasion of anti-parasitic effector mechanisms as mediators of the inflammatory response by T. gondii may be induced by brain ischemic tolerance [26]. The HIF family as master regulatory transcription factors upregulate multiple genes controlling neovascularization [27].…”
Section: Control Toxomentioning
confidence: 99%
“…T. gondii preferentially infects host monocyte/macrophage lineage cells, such as microglia [ 22 ], and also contributes to the resolution of inflammation by releasing IL-10 and TGF-β (transforming growth factor-beta) through the differentiation of M2 phenotype macrophages [ 13 , 23 – 25 ]. The evasion of anti-parasitic effector mechanisms as mediators of the inflammatory response by T. gondii may be induced by brain ischemic tolerance [ 26 ].…”
Section: Introductionmentioning
confidence: 99%
“…In Iran, until now, most of the decisions on infected fetuses were made based on serological findings in their mothers, which might have led to abortion of many uninfected foetuses. [6] The low avidity of immunoglobulin G (IgG) has been reported to be a useful marker of recent infection with Toxoplasma . Nevertheless, discrepant results on the maturation of avidity over time have been reported.…”
Section: Introductionmentioning
confidence: 99%