T‐Cell Repertoire Analysis in Acute and Chronic Human Chagas'Disease: Differentail Frequencies of Vb5 Expressing T Cells

Costa, Ronaldo Peres; Gollob, Kenneth J.; Fonseca, Luis L.; Rocha, Manoel Otávio Costa; Chaves, A. S.; Medrano-Mercado, Nora; Araujo-Jorge, T. C.; Antas, Paulo Renato Zuquim; Corrêa-Oliveira, Rodrigo; Gazzinelli, G.; Carvalho-Parra, J. F.; Dutra, Walderez Ornelas

doi:10.1046/j.1365-3083.2000.00706.x

Cited by 39 publications

(54 citation statements)

References 29 publications

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“…Although studies of endomyocardial biopsies from acute patients have shown the presence of CD4+ and CD8+ T cells in the inflammatory myocarditis [29], the function of these cells during the acute phase has not been determined. Interestingly, a decreased frequency of a particular CD4+ T-cell subpopulation expressing the Vbeta 5 region of the T-cell receptor (TCR) was seen in acute Chagas patients [30]. We speculate that this decrease was due to an activation-induced cell death, since the frequency of this population is increased upon lowering of antigenic concentration in chronic patients.…”

Section: How the Early Encounter Of Trypanosoma Cruzi With Host Cellsmentioning

confidence: 93%

“…Studies regarding T-cell repertoire showed that CD4+ T cells from indeterminate and cardiac patients displayed preferential expression of the Vbeta 5 TCR region [30]. However, recent studies showed that while CD8+CD28+ T-cells from indeterminate patients preferentially express Vbeta 3.1 and 5, the same cell population isolated from severe cardiac patients displayed a preferential expression of Vbeta 3.1, but not Vbeta 5 [42].…”

Section: Immunoregulation In the Chronic Phase: Balancing Parasite Comentioning

confidence: 96%

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Current concepts in immunoregulation and pathology of human Chagas disease

Dutra¹,

Gollob

2008

Current Opinion in Infectious Diseases

113

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Purpose of review-Chagas disease is a complex ailment caused by infection with Trypanosoma cruzi. It afflicts millions in Latin America. Years of studies have focused on the development of pathology in Chagas disease and recent studies have helped us understand the cellular mechanisms behind differential clinical evolution of Chagas disease.Recent findings-We discuss recent findings concerning the cellular immune response in human Chagas disease focusing on immunoregulation and the development of pathology. We seek to put several findings into the context of a disease that initially controls an extreme and patent infection, and later progresses to a chronic phase marked by the presence (cardiac and digestive forms), or not (indeterminate form), of associated pathology.Summary-Several theories exist to explain differential clinical evolution of Chagas disease. A coherent understanding of these theories will certainly aid in determining what combination of them approximates the true development of chagasic pathology. For achieving the goal of developing a successful therapy or intervention, it is critical that no theory be excluded at this point, but. Rather, rather that a thoughtful analysis and assimilation of the best components of each system into a central theory that best fits the reality of human Chagas disease is desirable.

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Section: How the Early Encounter Of Trypanosoma Cruzi With Host Cellsmentioning

confidence: 93%

Section: Immunoregulation In the Chronic Phase: Balancing Parasite Comentioning

confidence: 96%

Current concepts in immunoregulation and pathology of human Chagas disease

Dutra¹,

Gollob

2008

Current Opinion in Infectious Diseases

113

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“…In human, decreased CD4 lymphocytes in Chagas patients was described ten years ago [136]. Thymic function appears to be affected in several ways by T. cruzi, including the expression of chemokines, extracellular matrix molecules and receptors [137] and disturbing the pre-T cells trafficking, but also the shaping of peripheral T cell repertoire that reveals changes both in infected mice and human [138][139][140]. As for HAARTtreated HIV infection, conjonction of thymotropism of pathogen, GH/IGF-1 axis disturbance and correlated effects on T immune system suggest that GH can be considered as an immunomodulating substance for boosting the T-cell system and controlling parasite replication, and a combination of GH with anti-infectious drugs could be a new therapeutic strategy to reduce the harmful effects of Chagas disease.…”

Section: Implications For Chagas Diseasementioning

confidence: 99%

Impact of the Somatotrope Growth Hormone (GH)/Insulin-Like Growth Factor 1 (IGF-1) Axis Upon Thymus Function: Pharmacological Implications in Regeneration of Immune Functions

Goffinet¹,

Mottet²,

Kermani³

et al. 2011

IEMAMC

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Abstract:The thymus is the central lymphoid structure where T-cell differentiation takes place, and a crucial organ for the maintenance of homeostasis in the immune system. Thymopoiesis includes intrathymic proliferation of T-cell precursors, selection and output of both self-tolerant and competent effector T cells, as well as of natural regulatory T cells (nTreg). In the crosstalk between the neuroendocrine and immune systems, peptide hormones have been more and more implicated in immunomodulation for the last thirty years. The somatotrope growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis in particular has been repeatedly shown to play a major regulatory role upon thymus function and T-cell development. This review will focus on the important thymotropic properties of the somatotrope GH/IGF-1 axis, and will try to discriminate these properties in function of the endocrine or paracrine/autocrine pathways involved in their mediation. Most importantly, in light of an increasing number of recent studies, GH and IGF-1 now appear as novel therapeutic agents that could be used for enhancing thymopoiesis in different cases of immune deficiencies, including aging-related immune dysfunction.Keywords: Thymus, growth hormone (GH), insulin-like growth factors (IGFs), HIV, growth hormone deficiency (GHD), Chagas disease. GENERAL INTRODUCTIONThe thymus is now considered as a crucial organ for maintenance of immune system homeostasis and the central lymphoid organ where occurs the generation of self-tolerant and competent naive T cells, as well as self-antigen specific natural Treg cells [1,2]. However, for a long time, the thymus has been regarded as an endocrine gland. In addition, the thymus now appears as a privileged site where the endocrine and immune systems intimately interact.A permanent crosstalk exists between the neuroendocrine and immune systems [3][4][5][6]. In addition to the strong modulation of immunity by glucocorticoids and sexual steroids, other hormones have been more and more involved in immunomodulation. Indeed, the somatotrope GH/IGF-1 axis, as well as prolactin and thyroid hormones [7], were shown to play an important regulatory role in T-cell development [8][9][10].GH is mainly synthesised in the anterior pituitary gland but can also be produced by immune cells [11,12]. GH has several biological actions in the immune system including regulation of thymopoiesis and T-cell development [13]. Nevertheless, it is uneasy to distinguish whether the thymotropic effects of GH are direct or mediated by IGF-1, as most *Address correspondence to this author at the University of Liege Center of Immunoendocrinology (CIL), Institute of Pathology CHU-B23, B-4000 Liege-Sart Tilman, Belgium; Tel: +32 43 66 25 50; Fax: +32 43 66 98 59; E-mail: vgeenen@ulg.ac.be of GH effects are driven by induction of IGF-1 and as IGF-1 has also been described as an endogenous factor in the thymic microenvironment [12]. The evolution of the research field has brought new insights that justify an overview update as some ancie...

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“…Recently, it was shown that functional anti-receptor antibodies bind to the second extracellular loop of the M2 muscarinic receptor [121]. It was also demonstrated that sera from chronic Chagas' disease patients interfere with electric and mechanical activities of embryonic myocardial cells in vivo [122,123]. These alterations in heart cell function seem to result from the previously demonstrated binding of antibodies to ~-adrenergic and M2-cholinergic receptors on the myocardial cell surface [122][123][124], and sera from CCC patients induce arrythmia in rabbit hearts [124].…”

Section: Autoantibodiesmentioning

confidence: 99%

“…It was also demonstrated that sera from chronic Chagas' disease patients interfere with electric and mechanical activities of embryonic myocardial cells in vivo [122,123]. These alterations in heart cell function seem to result from the previously demonstrated binding of antibodies to ~-adrenergic and M2-cholinergic receptors on the myocardial cell surface [122][123][124], and sera from CCC patients induce arrythmia in rabbit hearts [124]. Authors have demonstrated that the presence of such functionally active anti-receptor antibodies does not correlate with heart symptomatology but rather with dysfunction of the autonomic nervous system [121].…”

Section: Autoantibodiesmentioning

confidence: 99%