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2030-01-01
Objetivos de Desarrollo Sostenible
03 Saúde e Bem-EstarColecciones
- IOC - Artigos de Periódicos [12708]
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IMMUNOENDOCRINOLOGY OF THE THYMUS IN CHAGAS DISEASE
Fator de Necrose Tumoral alfa
Glucocorticoides
Linfócitos T Reguladores
Atrofia do timo
Autor
Afiliación
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina.
Instituto Nacional de Câncer. Departamento de Pesquisa Clínica. Rio de Janeiro, RJ, Brasil.
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina / Inter-American Open University. School of Medicine. Department of Physiology. Rosario, Argentina.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo Rio de Janeiro, RJ. Brasil.
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina.
Universidade de São Paulo. Escola de Medicina de Ribeirão Preto. Departamento de Bioquímica e Imunologia. Ribeirão Preto, SP, Brasil
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo Rio de Janeiro, RJ. Brasil.
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina.
Instituto Nacional de Câncer. Departamento de Pesquisa Clínica. Rio de Janeiro, RJ, Brasil.
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina / Inter-American Open University. School of Medicine. Department of Physiology. Rosario, Argentina.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo Rio de Janeiro, RJ. Brasil.
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina.
Universidade de São Paulo. Escola de Medicina de Ribeirão Preto. Departamento de Bioquímica e Imunologia. Ribeirão Preto, SP, Brasil
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo Rio de Janeiro, RJ. Brasil.
National University of Rosario. Faculty of Medical Sciences. Institute of Immunology. Rosario, Argentina.
Resumen en ingles
During immune response to infectious agents, the host develops an inflammatory response which could fail to eliminate the pathogen or may become dysregulated. In this case, the ongoing response acquires a new status and turns out to be detrimental. The same elements taking part in the establishment and regulation of the inflammatory response (cytokines, chemokines, regulatory T cells and counteracting compounds like glucocorticoids) may also mediate harmful effects. Thymic disturbances seen during Trypanosoma cruzi (T. cruzi) infection fit well with this conceptual framework. After infection, this organ suffers a severe atrophy due to apoptosis-induced thymocyte exhaustion, mainly affecting the immature double-positive (DP) CD4+CD8+ population. Thymus cellularity depletion, which occurs in the absence of main immunological mediators involved in anti-T. cruzi defense, seems to be linked to a systemic cytokine/hormonal imbalance, involving a dysregulated increase in Tumor Necrosis Factor alpha (TNF-α) and corticosterone hormone levels. Additionally, we have found an anomalous exit of potentially autoimmune DP cells to the periphery, in parallel to a shrinkage in the compartment of natural regulatory T cells. In this context, our data clearly point to the view that the thymus is a target organ of T. cruzi infection. Preserved thymus may be essential for the development of an effective immune response against T. cruzi, but this organ is severely affected by a dysregulated circuit of proinflammatory cytokines and glucocorticoids. Also, the alterations observed in the DP population might have potential implications for the autoimmune component of human Chagas disease.
Palabras clave en portugues
Doença de ChagasFator de Necrose Tumoral alfa
Glucocorticoides
Linfócitos T Reguladores
Atrofia do timo
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