Role of gamma interferon inToxoplasma gondii infection

Subauste, Carlos S.; Remington, J S

doi:10.1007/bf01964408

Cited by 52 publications

(20 citation statements)

References 76 publications

(43 reference statements)

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“…There is abundant evidence that IFN-␥ is the major cytokine involved in activation of macrophages and neutrophils to a candidacidal stage (3,9). The administration of IFN-␥ to mice beneficially influences the course of experimental infection with various pathogens, such as Toxoplasma gondii (32), Leishmania major (17), Trypanosoma cruzi (6), and Pneumocystis murina (30). In most models, macrophages and/or neutrophils are the main effector cells of IFN-␥-stimulated microbicidal activity.…”

Section: Discussionmentioning

confidence: 99%

Impairment of Host Defense against Disseminated Candidiasis in Mice Overexpressing GATA-3

Haraguchi¹,

Ishii²,

Morishima³

et al. 2010

Infect Immun

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Candida species are the most common source of nosocomial invasive fungal infections. Previous studies have indicated that T-helper immune response is the critical host factor for susceptibility to Candida infection. The transcription factor GATA-3 is known as the master regulator for T-helper type 2 (Th2) differentiation. We therefore investigated the role of GATA-3 in the host defense against systemic Candida infection using GATA-3-overexpressing transgenic mice. The survival of GATA-3-overexpressing mice after Candida infection was significantly lower than that of wild-type mice. Candida outgrowth was significantly increased in the kidneys of GATA-3-overexpressing mice, compared with wild-type mice. The levels of various Th2 cytokines, including interleukin-4 (IL-4), IL-5, and IL-13, were significantly higher while the level of Th1 cytokine gamma interferon was significantly lower in the splenocytes of GATA-3-overexpressing mice after Candida infection. Recruitment of macrophages into the peritoneal cavity in response to Candida infection and their phagocytic activity were significantly lower in GATA-3-overexpressing mice than in wild-type mice. Exogenous administration of gamma interferon to GATA-3-overexpressing mice significantly reduced Candida outgrowth in the kidney and thus increased the survival rate. Administration of gamma interferon also increased the recruitment of macrophages into the peritoneal cavity in response to Candida infection. These results indicate that overexpression of GATA-3 modulates macrophage antifungal activity and thus enhances the susceptibility to systemic Candida infection, possibly by reducing the production of gamma interferon in response to Candida infection.

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Section: Discussionmentioning

confidence: 99%

Impairment of Host Defense against Disseminated Candidiasis in Mice Overexpressing GATA-3

Haraguchi¹,

Ishii²,

Morishima³

et al. 2010

Infect Immun

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“…We previously reported that T cells play a major role in mediating protective immunity against low-and high-virulence strains of T. gondii from studies that depleted T cells in vivo with a mAb against Thyl.2 (11). Further evidence comes from the finding that interferon y released from sensitized T cells acts as a major mediator of the host defenses against T. gondii infection (19,20). Taking these results together, one might suggest that the expression of HSPs in mice immunized by Toxoplasma cell homogenates may be attributable to cytok-ines like interferon y.…”

Section: Discussionmentioning

confidence: 99%

Induction of heat shock protein closely correlates with protection against Toxoplasma gondii infection.

Nagasawa¹,

Oka²,

Maeda³

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

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Heat shock proteins (HSPs) are evolutionarily highly conserved polypeptides that appear to be produced by many cells to preserve cellular functions under a variety of conditions of stress, including infections. We report that a 65-kDa HSP is present in mouse peritoneal cells that have been infected with a low-virulence (Beverley) strain of Toxoplasma gondii, as determined by electroblot assay using a monoclonal antibody specific for microbial HSP65. This HSP is, however, not expressed when infection occurs with the high-virulence

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“…Interferon γ is clearly important in the control of infection. INFγ knockout mice cannot control infection and anti-INFγ can cause reactivation encephalitis in chronically infected mice (1,19,20).…”

Section: Introductionmentioning

confidence: 99%

The development and biology of bradyzoites of toxoplasma gondii

Weiss¹

2000

Front Biosci

113

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Toxoplasma gondii is a protozoan parasite of mammals and birds that is an important human pathogen. Infection with this Apicomplexan parasite results in its dissemination throughout its host via the tachyzoite life-stage. After dissemination these tachyzoites differentiate into bradyzoites within cysts that remain latent. These bradyzoites can transform back into tachyzoites and in immunosupressed individuals this often results in symptomatic disease. Both tachyzoites and bradyzoites develop in tissue culture and thus this crucial differentiation event can be studied. Recent advances in the genetic manipulation of T. gondii have expanded the molecular tools that can be applied to studies on bradyzoite differentiation. Evidence is accumulating that this differentiation event is stress mediated and may share common pathways with other stress-induced differentiation events in other eukaryotic organisms. Study of the stress response and signaling pathways are areas of active research in this organism. In addition, characterization of unique bradyzoite-specific structures, such as the cyst wall, should lead to a further understanding of T. gondii biology. This review focuses on the biology and development of bradyzoites and current approaches to the study of the tachyzoite to bradyzoite differentiation process.

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Role of gamma interferon inToxoplasma gondii infection

Cited by 52 publications

References 76 publications

Impairment of Host Defense against Disseminated Candidiasis in Mice Overexpressing GATA-3

Impairment of Host Defense against Disseminated Candidiasis in Mice Overexpressing GATA-3

Induction of heat shock protein closely correlates with protection against Toxoplasma gondii infection.

The development and biology of bradyzoites of toxoplasma gondii

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