Phenotypical characterization of regulatory T cells in acute Zika infection

Autor: Rephany Fonseca Peixoto, Tatjana Souza Lima Keesen, Cínthia Nóbrega de Sousa Dias, Daniel M. Altmann, Robson Cavalcante Veras, Pedro Henrique de Sousa Palmeira, Isabel Cristina Guerra-Gomes, Fátima de Lourdes Assunção Araújo de Azevedo, Josélio Maria Galvão de Araújo, Bárbara Guimarães Csordas, Rosemary J. Boyton, Isac Almeida de Medeiros, Bruna Macêdo Gois
Jazyk: angličtina
Rok vydání: 2021
Předmět:
Zdroj: Cytokine
Popis: Zika virus (ZIKV), alongside Dengue virus (DENV), Chikungunya virus (CHIKV), and Yellow Fever Virus (YFV) are prevalent arboviruses in the Americas. Each of these infections is associated with the development of associated disease immunopathology. Immunopathological processes are an outcome of counter-balancing impacts between effector and regulatory immune mechanisms. In this context, regulatory T cells (Tregs) are key in modulating the immune response and, therefore, in tissue damage control. However, to date, Treg phenotypes and mechanisms during acute infection of the ZIKV in humans have not been fully investigated. The main aim of this work was to characterize Tregs and their immunological profile related to cytokine production and molecules that are capable of controlling the exacerbated inflammatory profile in acute Zika infected patients. Using whole blood analyses of infected patients, an ex vivo phenotypical characterization of Tregs, circulating during acute Zika virus infection, was conducted by flow cytometry. We found that though there are no differences in absolute Treg frequency between infected and healthy control groups. However, pro-inflammatory cytokine up-regulation such as IFN-γ and LAP was observed in the acute disease. Furthermore, acute ZIKV patients expressed increased levels of CD39/CD73, perforin/granzyme B, PD-1, and CTLA-4, all markers involved in mechanisms used by Tregs to attempt to control strong inflammatory responses. Thus, the data indicates a potential contribution of Tregs during the inflammatory ZIKV infection response.
Databáze: OpenAIRE