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IL-10 overexpression predisposes to invasive aspergillosis by suppressing antifungal immunity

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Resumo:Proinflammatory immune responses are critically required for antimicrobial host defenses; however, excessive inflammation has the potential to damage host tissues thereby paradoxically contributing to the progression of infection. A central negative regulator of inflammatory responses is IL-10, an immunosuppressive cytokine with a wide variety of functions across multiple cell types. Although the role of IL-10 during infection appears to vary for different microorganisms, a largely detrimental role has been attributed to this cytokine during fungal disease. Given the variable risk of infection and its outcome among patients with comparable predisposing factors, susceptibility to invasive aspergillosis (IA) is thought to rely largely on genetic predisposition. The initial investigation of genetic variability at the IL10 locus led to the identification of single nucleotide polymorphisms (SNPs) influencing its transcriptional activity; thus, IL-10 may be a reasonable candidate for the genetic regulation of susceptibility to IA in high-risk patients.
Autores principais:Cunha, Cristina
Outros Autores:Gonçalves, Samuel M.; Duarte-Oliveira, Cláudio; Leite, Luís; Lagrou, Katrien; Marques, António; Lupiañez, Carmen B.; Mesquita, Inês; Gaifem, Joana; Barbosa, Ana Margarida; Pinho Vaz, Carlos; Branca, Rosa; Campilho, Fernando; Freitas, Fátima; Ligeiro, Dário; Lass-Flörl, Cornelia; Löffler, Jürgen; Jurado, Manuel; Saraiva, Margarida; Kurzai, Oliver; Rodrigues, Fernando; Castro, António G.; Silvestre, Ricardo; Sainz, Juan; Maertens, Johan A.; Torrado, Egídio; Jacobsen, Ilse D.; Lacerda, João; Campos, Jr, António; Carvalho, Agostinho
Ano:2017
País:Portugal
Tipo de documento:artigo
Tipo de acesso:acesso aberto
Instituição associada:Universidade de Lisboa
Idioma:inglês
Origem:Repositório da Universidade de Lisboa
Descrição
Resumo:Proinflammatory immune responses are critically required for antimicrobial host defenses; however, excessive inflammation has the potential to damage host tissues thereby paradoxically contributing to the progression of infection. A central negative regulator of inflammatory responses is IL-10, an immunosuppressive cytokine with a wide variety of functions across multiple cell types. Although the role of IL-10 during infection appears to vary for different microorganisms, a largely detrimental role has been attributed to this cytokine during fungal disease. Given the variable risk of infection and its outcome among patients with comparable predisposing factors, susceptibility to invasive aspergillosis (IA) is thought to rely largely on genetic predisposition. The initial investigation of genetic variability at the IL10 locus led to the identification of single nucleotide polymorphisms (SNPs) influencing its transcriptional activity; thus, IL-10 may be a reasonable candidate for the genetic regulation of susceptibility to IA in high-risk patients.