Characterization of the presence of Foxp3+ T cells from patients with different clinical forms of Chagas' disease

Myocardial Gene Expression ofT-bet,GATA-3,Ror-γt,FoxP3, and Hallmark Cytokines in Chronic Chagas Disease Cardiomyopathy: An Essentially Unopposed TH1-Type Response

“…Our finding of a modest increase in the mRNA expression of FoxP3 and CTLA-4, with no significant modulation of TGF- β and IL-10 expression, is in line with previous studies showing that FoxP3+ cells are significantly less abundant in myocardial sections from CCC than in ASY patients or noninfected individuals, suggesting that reduced numbers of Treg cells could be one important cause for the prevalent T H 1 response in CCC heart tissue [29]. Araujo et al [21] have previously shown that PBMC from CCC patients displayed increased numbers of CD4 + CD25 high Foxp3 + CTLA-4 + T cells and decreased numbers of CD4 + CD25 high IL-10 + T cells, as compared to ASY patients, consistent with our findings in regulatory T cell molecules in CCC heart tissue [22].…”

“…Although studies with PBMC have established significant differences in the frequency of functional T cell subset differences between CCC and ASY, it does not necessarily follow that those findings will all apply to CCC heart tissue. The presence of different Treg populations in CCC heart tissue has been suggested by the findings of Foxp3 expression and TGF- β signaling (through Smad4 detection) in CCC compared to ASY heart tissue [28, 29]. Regarding production of IL-4 in CCC myocardium, there are conflicting results, where IL-4-producing mononuclear cells were either undetectable [14], prominent in autopsy samples [25], or outnumbered by IFN- γ -producing T cells [30].…”

Regulatory T Cell and Forkhead Box Protein 3 as Modulators of Immune Homeostasis

“…In Chagas disease, a high frequency of FOXP3 + Treg was directly correlated with moderate inflammation, thus preventing the development of megacolon (253); a similar association was also found among patients with heart disease (254). While specific suppressor mechanisms are a continuing focus of research, the available data indicate that such cells modulate the cytokine microenvironment, IL-10 and IFN-γ in particular, and/or induce lysis of effector cells through a granzyme-dependent pathway in patients with the indeterminate form of Chagas disease (255).…”

Evaluation of Gene Expression of TGF-B and FOXP3 in Individuals Chronically Infected with Trypanosoma Cruzi

“…These cells are an important source of regulation of the immune response, controlling the local inflammatory response and avoiding severe tissue destruction [10]. According to Araujo et al, [11], patients presenting the CARD form have specific populations of CD8+ T cells, which results in the production of inflammatory cytokines. These cytokines may be involved in the establishment of an exacerbated inflammatory process, leading to an uncontrolled immune response.…”

“…The latter is characterized by the absence or in ability of action of regulatory T cells (Treg cells) through the production of their main cytokine, TGF-β, which modulates the expression of FOXP3 by Tregs and is also able to transform peripheral CD4+ CD25 -T cells in CD4+ CD25+ cells [12]. On the contrary, patients with the IND form have an effective, possibly transient, immune regulatory response that controls the response to infection mediated by regulatory effector T cells [11].…”