Diverse mechanisms employed by Toxoplasma gondii to inhibit IFN-γ-induced major histocompatibility complex class II gene expression

Lang, Christine; Algner, Michaela; Beinert, Nicole; Groß, Uwe; Lüder, Carsten G. K.

doi:10.1016/j.micinf.2006.02.031

Cited by 61 publications

(80 citation statements)

References 36 publications

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“…1A). On the other hand, IFN-␥-induced transcription of the genes, including both CD74 isoforms, was inhibited in infected cells, in agreement with previous reports showing inhibition of IFN-␥-mediated transcription by T. gondii (15,22,33,34).…”

Section: T Gondii Infection Inhibits Transcription Of Mhc-ii (H2) Andsupporting

confidence: 91%

“…Previous studies have reported transcriptional regulation of MHC-II and other, related genes in Toxoplasma-infected cells, whereby interferon gamma (IFN-␥)-induced transcription is inhibited in infected cells (15,33,34). Levels of MHC-II proteins are reduced in infected cells, antigen presentation is impaired, and priming and activation of CD4 ϩ T cells are greatly diminished (23,24,35), yet small amounts of MHC-II proteins are detected in these cells.…”

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confidence: 99%

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Parasite Manipulation of the Invariant Chain and the Peptide Editor H2-DM Affects Major Histocompatibility Complex Class II Antigen Presentation during Toxoplasma gondii Infection

et al. 2015

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Section: T Gondii Infection Inhibits Transcription Of Mhc-ii (H2) Andsupporting

confidence: 91%

mentioning

confidence: 99%

Parasite Manipulation of the Invariant Chain and the Peptide Editor H2-DM Affects Major Histocompatibility Complex Class II Antigen Presentation during Toxoplasma gondii Infection

et al. 2015

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“…gondii actively down-regulates the expression of major histocompatibility complex class I and class II molecules in murine macrophages and monocytes, which may directly inhibit their antigen-presenting capacity [15,21]. Apoptosis caused by parasite infection in splenocytes, including CD4 + and CD8 + lymphocytes, B lymphocytes, NK cells, and granulocytes, and in Peyer's patch T cells, may also contribute to suppression of the immune response [7,17].…”

Section: Discussionmentioning

confidence: 99%

Overproduction of the Pro-Apoptotic Molecule, Programmed Cell Death 5, in Toxoplasma gondii Leads to Increased Apoptosis of Host Macrophages

Bannai

Nishikawa

Ibrahim

et al. 2009

The Journal of Veterinary Medical Science

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ABSTRACT. We established a recombinant strain of Toxoplasma gondii that overexpressed programmed cell death 5 (TgPDCD5), in order to evaluate the role of endogenous TgPDCD5 in macrophage apoptosis during T. gondii infection. Immunofluorescence microscopy revealed that overproduced TgPDCD5 with a hemagglutinin tag was localized in the cytosol, which was consistent with the localization of endogenous TgPDCD5. The induced TgPDCD5-HA was recognized as an additional band by Western blot analysis, indicating successful overexpression of TgPDCD5. Secretion and release of TgPDCD5 by the parasite was also up-regulated in a time-dependent manner, which reflected its overproduction. Apoptosis due to parasite infection and interferon-gamma treatment was significantly upregulated by the overexpression of TgPDCD5. These results suggest that endogenous TgPDCD5 plays a role in macrophage apoptosis during T. gondii infection.

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“…In addition, STAT4-dependent IFN-γ has been reported in dendritic cells and macrophages [11]. Many reports have been shown the T. gondii success of toxoplasma's immune evasion strategies [10, 12,13]. The molecular basis of parasite-host interaction is important in understanding the disease mechanism and developed successful treatment strategy (Figure 2).…”

Section: Molecular Basis Of Toxoplasmosismentioning

confidence: 99%

Toxoplasmosis and Public Health Genomics

Oymak¹,

Merve²,

Sevilay³

et al. 2017

Toxoplasmosis

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Toxoplasma gondii infection generally causes flu-like symptoms in healthy individuals; however, immunosuppression of the infected individual causes reactivation of the pathogen to its active form and relapse of the toxoplasmosis. Today it is known that toxoplasmosis triggers psychiatric disorders such as schizophrenia as well as behavioral changes such as suicide attempts. Although dermatological manifestations are very rare, the dermatological lesions are not unique. In addition, previous toxoplasma infection also causes congenital infections because of placental infection and causes birth defects and spontaneous abortion. T. gondii strains are mainly divided into three main clonal lineages, yet higher recombination rate causes unusual population structure and heterogeneous distribution of the pathogen. Both genetic variations, of the pathogen and the patients, are important for virulence property and success of the therapies. The scientist focuses on the genetic variations of the pathogens and individuals to achieve effective treatment and developed tailor-made medicines. Thus, understanding the molecular basis of the disease and the link of molecular mechanism with host immunity is important to fully know the disease and related disorders. In this chapter, we would like to evaluate the current knowledge on genetic, molecular characteristics of toxoplasmosis in view of public health genomics.

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Diverse mechanisms employed by Toxoplasma gondii to inhibit IFN-γ-induced major histocompatibility complex class II gene expression

Cited by 61 publications

References 36 publications

Parasite Manipulation of the Invariant Chain and the Peptide Editor H2-DM Affects Major Histocompatibility Complex Class II Antigen Presentation during Toxoplasma gondii Infection

Parasite Manipulation of the Invariant Chain and the Peptide Editor H2-DM Affects Major Histocompatibility Complex Class II Antigen Presentation during Toxoplasma gondii Infection

Overproduction of the Pro-Apoptotic Molecule, Programmed Cell Death 5, in Toxoplasma gondii Leads to Increased Apoptosis of Host Macrophages

Toxoplasmosis and Public Health Genomics

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