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CD8(+) tissue-resident memory T-cell development depends on infection-matching regulatory T-cell types

Immunological memory is critical for immune protection, particularly at epithelial sites, which are under constant risk of pathogen invasions. To counter invading pathogens, CD8(+) memory T cells develop at the location of infection: tissue-resident memory T cells (T(RM)). CD8(+) T-cell responses ar...

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Detalles Bibliográficos
Autores principales: Barros, Leandro, Piontkivska, Daryna, Figueiredo-Campos, Patrícia, Fanczal, Júlia, Ribeiro, Sofia Pereira, Baptista, Marta, Ariotti, Silvia, Santos, Nuno, Amorim, Maria João, Pereira, Cristina Silva, Veldhoen, Marc, Ferreira, Cristina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10495327/
https://www.ncbi.nlm.nih.gov/pubmed/37696824
http://dx.doi.org/10.1038/s41467-023-41364-w
Descripción
Sumario:Immunological memory is critical for immune protection, particularly at epithelial sites, which are under constant risk of pathogen invasions. To counter invading pathogens, CD8(+) memory T cells develop at the location of infection: tissue-resident memory T cells (T(RM)). CD8(+) T-cell responses are associated with type-1 infections and type-1 regulatory T cells (T(REG)) are important for CD8(+) T-cell development, however, if CD8(+) T(RM) cells develop under other infection types and require immune type-specific T(REG) cells is unknown. We used three distinct lung infection models, to show that type-2 helminth infection does not establish CD8(+) T(RM) cells. Intracellular (type-1) and extracellular (type-3) infections do and rely on the recruitment of response type-matching T(REG) population contributing transforming growth factor-β. Nevertheless, type-1 T(REG) cells remain the most important population for T(RM) cell development. Once established, T(RM) cells maintain their immune type profile. These results may have implications in the development of vaccines inducing CD8(+) T(RM) cells.