Programmed T-cell death in experimental chagas disease

DosReis, George A.; Fonseca, M. E. F.; Lopes, Marcela F.

doi:10.1016/0169-4758(95)80011-5

Cited by 40 publications

(27 citation statements)

References 40 publications

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“…Lymphocyte apoptosis may derive from the powerful polyclonal lymphocyte activation triggered by the infection, i.e, it may result from the hosts own regulatory needs (30). This proposal is consistent with the propriocide hypothesis of mature T-cell apoptosis, following engagement of the T-cell receptor (TCR) in actively cycling cells (31).…”

Section: Host Cell Apoptosis In Parasitic Infections and Its Pathogensupporting

confidence: 67%

“…Recent evidence indicates that phagocytosis of apoptotic T cells increases T. cruzi growth in macrophages in vitro and exacerbates parasitemia in vivo (Freire-de-Lima CG, DosReis GA and Lopes MF, unpublished results). One important remaining issue about apoptosis in Chagas disease is whether it plays a role in the tissue lesions found in the heart tissue of the host (30).…”

Section: Host Cell Apoptosis In Parasitic Infections and Its Pathogenmentioning

confidence: 99%

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Apoptosis in parasites and parasite-induced apoptosis in the host immune system: a new approach to parasitic diseases

Barcinski

DosReis

1999

Braz J Med Biol Res

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Apoptosis, a form of programmed cell death (PCD), has been described as essential for normal organogenesis and tissue development, as well as for the proper function of cell-renewal systems in adult organisms. Apoptosis is also pivotal in the pathogenesis of several different diseases. In this paper we discuss, from two different points of view, the role of apoptosis in parasitic diseases. The description of apoptotic death in three different species of heteroxenic trypanosomatids is reviewed, and considerations on the phylogenesis of apoptosis and on the eventual role of PCD on their mechanism of pathogenesis are made. From a different perspective, an increasing body of evidence is making clear that regulation of host cell apoptosis is an important factor on the definition of a host-pathogen interaction. As an example, the molecular mechanisms by which Trypanosoma cruzi is able to induce apoptosis in immunocompetent cells, in a murine model of Chagas disease, and the consequences of this phenomenon on the outcome of the experimental disease are discussed.

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Section: Host Cell Apoptosis In Parasitic Infections and Its Pathogensupporting

confidence: 67%

Section: Host Cell Apoptosis In Parasitic Infections and Its Pathogenmentioning

confidence: 99%

Apoptosis in parasites and parasite-induced apoptosis in the host immune system: a new approach to parasitic diseases

Barcinski

DosReis

1999

Braz J Med Biol Res

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“…On one hand, infectious agents manipulate host cell apoptosis either to increase their life span within infected cells or to spread infection. On the other hand, the host immune response induces apoptosis of infected target cells in order to damage intracellular microbial pathogens (4,14).…”

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confidence: 99%

Regulated Expression and Effect of Galectin-1 onTrypanosoma cruzi-Infected Macrophages: Modulation of Microbicidal Activity and Survival

et al. 2001

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Galectin-1 is a ␤-galactoside-binding protein with potent anti-inflammatory and immunoregulatory effects. However, its expression and function have not been assessed in the context of an infectious disease. The present study documents, for the first time, the regulated expression of galectin-1 in the context of an infectious process and its influence in the modulation of macrophage microbicidal activity and survival. A biphasic modulation in parasite replication and cell viability was observed when macrophages isolated from Trypanosoma cruziinfected mice were exposed to increasing concentrations of galectin-1. While low concentrations of this protein increased parasite replication and did not affect macrophage survival, higher inflammatory doses of galectin-1 were able to commit cells to apoptosis and inhibited parasite replication. Furthermore, galectin-1 at its lowest concentration was able to down-regulate critical mediators for parasite killing, such as interleukin 12 (IL-12) and nitric oxide, while it did not affect IL-10 secretion. Finally, endogenous galectin-1 was found to be up-regulated and secreted by the J774 macrophage cell line cultured in the presence of trypomastigotes. This result was extended in vivo by Western blot analysis, flow cytometry, and reverse transcription-PCR using macrophages isolated from T. cruzi-infected mice. This study documents the first association between galectin-1's immunoregulatory properties and its role in infection and provides new clues to the understanding of the mechanisms implicated in host-parasite interactions during Chagas' disease and other parasite infections.

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“…In addition, signs of apoptosis have been detected in myocardial tissue from dogs infected with T. cruzi (Zhang et al 1999) and also in T cells and thymus nursing cells from T. cruzi-infected mice (DosReis et al 1995, Barcinski and DosReis 1999, DosReis and Barcinski 2001, Mucci et al 2002, De Souza et al 2003. Studies performed with heart tissue from chronic chagasic patients have been conflictive in their identification of apoptotic myocardial cells at inflammatory sites Souza 1999, Tostes et al 2005).…”

Section: Apoptosis Of Myocardial Cellsmentioning

confidence: 99%

Mechanisms of pathogenesis in Chagas disease

Kierszenbaum

2007

Acta Parasitologica

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Chagas disease, caused by the obligate unicellular parasite Trypanosoma cruzi, presents itself in a diverse collection of clinical manifestations, ranging from severe, fatal heart and digestive tract pathologies to unapparent or minor alterations that do not compromise survival. Over the years, a number of mechanisms have been proposed to explain the pathogenesis of chagasic tissue lesions, all of which have faced some criticism or been received with skepticism. This article excludes the autoimmunity hypothesis for Chagas disease because it has been extensively reviewed elsewhere, and summarizes the various alternative hypotheses that have been advanced over the years. For each of these hypotheses, an outline of its main tenets and key findings that support them is presented. This is followed by the results and comments that have challenged them and the caveats that stand on their way to wider acceptance. It is hoped that this writing will draw attention to our shortcomings in understanding the pathogenesis of Chagas disease, which, unfortunately, continues to figure among the most serious health problems of the American continent.

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Programmed T-cell death in experimental chagas disease

Cited by 40 publications

References 40 publications

Apoptosis in parasites and parasite-induced apoptosis in the host immune system: a new approach to parasitic diseases

Apoptosis in parasites and parasite-induced apoptosis in the host immune system: a new approach to parasitic diseases

Regulated Expression and Effect of Galectin-1 onTrypanosoma cruzi-Infected Macrophages: Modulation of Microbicidal Activity and Survival

Mechanisms of pathogenesis in Chagas disease

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