RESUMO
Regulatory T cells (Tregs ) constitute a fascinating subpopulation of CD4(+) T cells due to their ability to limit the immune response against self and non-self antigens. Murine models and antibodies directed against surface and intracellular molecules have allowed elucidation of the mechanisms that govern their development and function. However, these markers used to their classification lack of specificity, as they can be expressed by activated T cells. Similarly, there are slight differences between animal models, in steady state and pathological conditions, anatomical localization and strategy of analysis by flow cytometry. Here, we revised the most common markers utilized for Treg typification by flow cytometry such as CD25, forkhead box protein 3 (FoxP3) and CD127, along with our data obtained in different body compartments of humans, mice and rats. Furthermore, we revised and determined the expression of other molecules important for the phenotypical characterization of Treg cells. We draw attention to the drawbacks of those markers used in chronic states of inflammation. However, until a specific marker for the identification of Tregs is discovered, the best combination of markers will depend upon the tissue or the degree of inflammation from which Tregs derive.
Assuntos
Linfócitos T Reguladores/imunologia , Linfócitos T Reguladores/fisiologia , Animais , Biomarcadores/metabolismo , Antígenos CD4/metabolismo , Citometria de Fluxo , Fatores de Transcrição Forkhead/genética , Fatores de Transcrição Forkhead/metabolismo , Humanos , Inflamação/imunologia , Linfonodos/imunologia , Ativação Linfocitária , Camundongos , Fenótipo , Ratos , Baço/citologia , Baço/imunologiaRESUMO
To determine whether fibroblasts from Blanco Orejinegro cattle, exhibit any level of resistance to infection against vesicular stomatitis virus (VSV) serotypes Indiana (VSV-I) or New Jersey (VSV-NJ), 30 fibroblast cultures were phenotyped to evaluate their resistance/susceptibility. Thirty three % of Blanco Orejinegro fibroblast cultures were classified as very resistant, 50% as resistant, and 17% as susceptible to VSV-I infection, whereas 20% were classified as very resistant, 50% as resistant and 30% as susceptible to VSV-NJ infection. Therefore, there appears to be a large variation in phenotypic polymorphism among the fibroblasts to infection by VSV. To elucidate the mechanisms responsible for this diversity, we searched for a possible relationship between resistance/ susceptibility and production of factors wi th antiviral activity; however fibroblasts did not secrete factors with antiviral activity. We examined also whether apoptosis where induced by infection and its correlation with the polymorphism of resistance/susceptibility to VSV. Using morphological analyses, hypoploidy measurements, and level of phosphatidyl serine expression, high levels of apoptosis were measured in VSV infected fibroblasts. However, no correlation exists between apoptosis and the category of resistance/susceptibility to infection, indicating that apoptosis is a pathogenic mechanism of VSV.(AU)
Assuntos
Bovinos , Animais , Antivirais/metabolismo , Membrana Celular/metabolismo , Fibroblastos/patologia , Fibroblastos/virologia , Fosfatidilserinas/metabolismo , Infecções por Rhabdoviridae/patologia , Infecções por Rhabdoviridae/virologia , Frações Subcelulares/metabolismo , Apoptose , Forma Celular , Células Cultivadas , Fenótipo , PloidiasRESUMO
To determine whether fibroblasts from Blanco Orejinegro cattle, exhibit any level of resistance to infection against vesicular stomatitis virus (VSV) serotypes Indiana (VSV-I) or New Jersey (VSV-NJ), 30 fibroblast cultures were phenotyped to evaluate their resistance/susceptibility. Thirty three % of Blanco Orejinegro fibroblast cultures were classified as very resistant, 50% as resistant, and 17% as susceptible to VSV-I infection, whereas 20% were classified as very resistant, 50% as resistant and 30% as susceptible to VSV-NJ infection. Therefore, there appears to be a large variation in phenotypic polymorphism among the fibroblasts to infection by VSV. To elucidate the mechanisms responsible for this diversity, we searched for a possible relationship between resistance/ susceptibility and production of factors wi th antiviral activity; however fibroblasts did not secrete factors with antiviral activity. We examined also whether apoptosis where induced by infection and its correlation with the polymorphism of resistance/susceptibility to VSV. Using morphological analyses, hypoploidy measurements, and level of phosphatidyl serine expression, high levels of apoptosis were measured in VSV infected fibroblasts. However, no correlation exists between apoptosis and the category of resistance/susceptibility to infection, indicating that apoptosis is a pathogenic mechanism of VSV.
Assuntos
Bovinos , Animais , Antivirais/metabolismo , Fibroblastos/patologia , Fibroblastos/virologia , Fosfatidilserinas/metabolismo , Frações Subcelulares/metabolismo , Infecções por Rhabdoviridae/patologia , Infecções por Rhabdoviridae/virologia , Membrana Celular/metabolismo , Apoptose , Forma Celular , Células Cultivadas , Fenótipo , PloidiasRESUMO
BACKGROUND: Apoptosis, also known as programmed cell death, has been reported not only as a pathogenic mechanism, but also as a mechanism of resistance and control of a variety of infections. Particularly during HIV-1 infection, apoptosis is the main mechanism by which infected and uninfected CD4+ lymphocytes are eliminated. However, apoptosis as a mechanism of natural resistance to HIV infection has this far not been explored. OBJECTIVE: To determine whether apoptosis could explain, at least in part, the natural resistance to HIV infection observed in some exposed but uninfected individuals (ESN). RESULTS: Our data shows that peripheral blood monocytes in the ESN group has a predisposition to undergo spontaneous apoptosis, as well as apoptosis induced by HIV infection in vitro, compared with monocyte population from the control group at low risk of HIV infection. CONCLUSIONS: These findings suggest that, in some ESN individuals, monocytes could play an important role in the control of HIV infection by undergoing apoptosis. However, since the variability among individuals is large, studies with larger cohorts focusing in monocyte apoptosis as pathogenic mechanisms are required.