Advances in understanding immunity to Toxoplasma gondii

Tait, Elia D.; Hunter, Christopher A.

doi:10.1590/s0074-02762009000200013

Cited by 44 publications

(35 citation statements)

References 131 publications

(103 reference statements)

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“…Because tachyzoites infect any cell type and tissue and replication leads to cell lysis, this parasite has a tremendous potential to cause disease. The innate immune response limits parasite growth and promotes the development of adaptive immunity, which is required for long term resistance to infection (2,5). In turn, T. gondii interferes with the host signaling pathways in the infected cells, enabling the parasite to evade the innate immune response.…”

mentioning

confidence: 99%

Toxoplasma gondii Virulence Factor ROP18 Inhibits the Host NF-κB Pathway by Promoting p65 Degradation

Chen

et al. 2014

Journal of Biological Chemistry

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Background: ROP18 is a Toxoplasma secreted Ser/Thr protein kinase important for acute virulence. Results: ROP18 phosphorylates host p65 at Ser-468 and target this protein to the ubiquitin-dependent degradation. Conclusion: ROP18 inhibits the host NF-B pathway by promoting p65 degradation. Significance: These findings reveal a novel molecular mechanism by which type I strain manipulates the host immune system to facilitate infection.

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mentioning

confidence: 99%

Toxoplasma gondii Virulence Factor ROP18 Inhibits the Host NF-κB Pathway by Promoting p65 Degradation

Chen

et al. 2014

Journal of Biological Chemistry

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“…The adaptive immune response is initiated by antigen-presenting cells (APCs), which recognize that the host is infected through pattern recognition receptors such as TLRs, stimulating secretion of IL-12, which induces IFN-γ production by NK cells and CD4 + and CD8 + T cells (Tait and Hunter 2009). Activated CD4+ cells produce IL-2, a T-cell mitogen, which in conjunction with IFN-γ, results in large numbers of parasite-specific CD4 + and CD8 + T cells that produce IFN-γ at the sites of parasite invasion.…”

Section: Immune Responsementioning

confidence: 99%

Toxoplasmosis

Halonen,

Weiss

2013

Neuroparasitology and Tropical Neurology

291

252

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Toxoplasma gondii, an Apicomplexan, is a pathogen that can infect the central nervous system. Infection during pregnancy can result in a congenial infection with severe neurological sequela. In immune compromised individuals reactivation of latent neurological foci can result in encephalitis. Immune competent individuals infected with T. gondii are typically asymptomatic and maintain this infection for life. However, recent studies suggest that these asymptomatic infections may have effects on behavior and other physiological processes. T. gondii infects approximately one-third of the world population, making it one of the most successful parasitic organisms. Cats and other felidae serve as the definite host producing oocysts, an environmentally resistant life cycle stage found in cat feces, which can transmit the infection when ingested orally. A wide variety of warm-blooded animals, including humans, can serve as the intermediate host in which tissue cysts (containing bradyzoites) develop. Transmission also occurs due to ingestion of the tissue cysts. There are 3 predominant clonal lineages, termed types I, II and III and an association with higher pathogenicity with the Type I strains in humans has emerged. This chapter presents a review of the biology of this infection including the life cycle, transmission, epidemiology, parasite strains, and the host immune response. The major clinical outcomes of congenital infection, chorioretinitis, and encephalitis, and the possible association of infection of toxoplasmosis with neuropsychriatric disorders such as schizophrenia, are reviewed.

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“…Hem akut, hem de kronik toksoplazmozun kontrolünde Th1 tipi yanıt en önemli rolü oynamaktadır 7,8 . AmE, IFN-γ ve IL-2 gibi Th1 sitokinlerinin üretimini artırarak parazitin çoğalmasını önleme etkisine sahiptir 12 .…”

Section: Mi̇krobi̇yoloji̇ Bülteni̇unclassified

“…Toksoplazmoza karşı konak savunmasında hücresel ve hümoral immün yanıt birlikte rol oynamakta ve hem insan hem de hayvanlarda akut toksoplazmoza karşı dirençte NK ve Th1 hücreleri ile antikorların önem taşıdığı bilinmektedir 7 . Bu hücrelerin etkileri; interlökin (IL)-1, IL-2, IL-12, interferon-gama (IFN-γ) ve tümör nekroz faktörü (TNF)-α gibi proinfl amatuvar sitokinleri salgılamaları sonucu ortaya çıkar 7,8 . Yapılan çalışmalarda toksoplazmoza karşı en etkili sitokinin IFN-γ olduğu; IFN-γ etkisiyle IL-12, IL-2 ve IL-7 sitokinlerinin de indirekt olarak salgılandığı ve toksoplazmoza karşı koruyucu etkilerinin olduğu gösterilmiştir 9 .…”

Section: Introductionunclassified