Author(s):
Cunha, Cristina ; 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
Date: 2017
Persistent ID: http://hdl.handle.net/10451/55225
Origin: Repositório da Universidade de Lisboa
Project/scholarship:
info:eu-repo/grantAgreement/FCT/FARH/SFRH%2FBPD%2F96176%2F2013/PT;
Description
© 2017 American Academy of Allergy, Asthma & Immunology
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.
Supported by the Northern Portugal Regional Operational Programme (NORTE 2020), under the Portugal 2020 Partnership Agreement, through the European Regional Development Fund (FEDER) (NORTE-01-0145-FEDER-000013), the Fundação para a Ciência e Tecnologia (FCT) (contracts IF/00735/2014 to A.C., IF/01390/2014 to E.T., IF/00021/2014 to R.S., and SFRH/BPD/96176/2013 to C.C.), the Conselho de Reitores das Universidades Portuguesas (CRUP), Portugal (Ações Integradas Luso-Alemãs A-43/16), the Deutscher Akademischer Austauschdienst (DAAD) (project-ID 57212690), the Fondo de Investigaciones Sanitarias (Madrid, Spain) (grant #PI12/02688) and the ERA-NET PathoGenoMics (grant #0315900A).
