| Texto completo | |
| Autor(es): |
Boldrini, Vinicius de Oliveira
[1, 2, 3]
;
Farias, Alessandro dos Santos
[1, 2, 3]
;
Degasperi, Giovanna Rosa
[4]
Número total de Autores: 3
|
| Afiliação do(s) autor(es): | [1] Univ Estadual Campinas, Inst Biol, Dept Genet Microbiol & Immunol, Autoimmune Res Lab, Campinas, SP - Brazil
[2] Univ Estadual Campinas, Inst Biol, Dept Genet Evolut Microbiol & Immunol, Neuroimmunol Unit, Campinas, SP - Brazil
[3] Natl Inst Sci & Technol Neuroimmunomodulat INCT N, Rio De Janeiro - Brazil
[4] Pontificia Univ Catolica Campinas PUC Campinas, Campinas, SP - Brazil
Número total de Afiliações: 4
|
| Tipo de documento: | Artigo de Revisão |
| Fonte: | Scandinavian Journal of Immunology; v. 90, n. 4 JULY 2019. |
| Citações Web of Science: | 0 |
| Resumo | |
Evidence indicates that reprogramming of metabolism is critically important for the differentiation of CD4 + T lymphocytes, and the manipulation of metabolic pathways in these cells may shape their fate and function. Distinct subgroups from T lymphocytes, such as Th17, adopt specific metabolic programmes to support their needs. Some important metabolic reactions, such as glycolysis, oxidative phosphorylation, are considered important for the differentiation of these lymphocytes. Since their discovery nearly a decade ago, Th17 lymphocytes have received significant attention because of their role in the pathology of several immune-mediated inflammatory diseases such as multiple sclerosis. In this review, it will be discussed as the involvement of T cell metabolism and as metabolic reprogramming in activated T cells dictates fate decisions to Th17. The involvement of nuclear receptors such as RORyt e PPARs in the induction of Th17 cells was also discussed. Understanding the metabolic pathways involved in the differentiation of the distinct subgroups of T lymphocytes helps in the design of promising therapeutic proposals. (AU) | |
| Processo FAPESP: | 17/21363-5 - Regulação da via JAK/STAT/SOCS na mudança de perfil de Th17 para Th1 (produtoras de IFNg) durante a evolução clínica da encefalomielite experimental autoimune |
| Beneficiário: | Alessandro dos Santos Farias |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |