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Modulation of regulatory T cell function and stability by co-inhibitory receptors.
Lucca, Liliana E; Dominguez-Villar, Margarita.
Afiliação
  • Lucca LE; Departments of Neurology and Immunobiology, Yale School of Medicine, New Haven, CT, USA.
  • Dominguez-Villar M; Faculty of Medicine, Imperial College London, London, UK. m.dominguez-villar@imperial.ac.uk.
Nat Rev Immunol ; 20(11): 680-693, 2020 11.
Article em En | MEDLINE | ID: mdl-32269380
ABSTRACT
Regulatory T (Treg) cells constitute a dynamic population that is essential for controlling immune responses in health and disease. Defects in Treg cell function and decreases in Treg cell numbers have been observed in patients with autoimmunity and the opposite effects on Treg cells occur in cancer settings. Current research on new therapies for these diseases is focused on modulating Treg cell function to increase or decrease suppressive activity in autoimmunity and cancer, respectively. In this regard, several co-inhibitory receptors that are preferentially expressed by Treg cells under homeostatic conditions have recently been shown to control Treg cell function and stability in different disease settings. These receptors could be amenable to therapeutic targeting aimed at modulating Treg cell function and plasticity. This Review summarizes recent data regarding the role of co-inhibitory molecules in the control of Treg cell function and stability, with a focus on their roles and potential therapeutic use in autoimmunity and cancer.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Linfócitos T Reguladores / Receptores Coestimuladores e Inibidores de Linfócitos T / Antineoplásicos Imunológicos / Neoplasias Limite: Animals / Humans Idioma: En Ano de publicação: 2020 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Linfócitos T Reguladores / Receptores Coestimuladores e Inibidores de Linfócitos T / Antineoplásicos Imunológicos / Neoplasias Limite: Animals / Humans Idioma: En Ano de publicação: 2020 Tipo de documento: Article