IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population (2017)
- Authors:
- USP affiliated authors: BORGES, MARCOS DE CARVALHO - FMRP ; ZAMBONI, DARIO SIMÕES - FMRP ; CUNHA, FERNANDO DE QUEIROZ - FMRP ; ALVES FILHO, JOSÉ CARLOS FARIAS - FMRP
- Unidade: FMRP
- DOI: 10.1038/ncomms14919
- Subjects: IMUNOSSUPRESSÃO; INTERLEUCINAS; PACIENTES; SEPSE
- Language: Inglês
- Imprenta:
- Source:
- Título: Nature Communications
- ISSN: 2041-1723
- Volume/Número/Paginação/Ano: v. 8, art. 14919, 2017
- Este periódico é de acesso aberto
- Este artigo é de acesso aberto
- URL de acesso aberto
- Cor do Acesso Aberto: gold
- Licença: cc-by
-
ABNT
NASCIMENTO, Daniele C. et al. IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population. Nature Communications, v. 8, 2017Tradução . . Disponível em: https://doi.org/10.1038/ncomms14919. Acesso em: 05 out. 2024. -
APA
Nascimento, D. C., Melo, P. H., Piñeros, A. R., Ferreira, R. G., Colón, D. F., Donate, P. B., et al. (2017). IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population. Nature Communications, 8. doi:10.1038/ncomms14919 -
NLM
Nascimento DC, Melo PH, Piñeros AR, Ferreira RG, Colón DF, Donate PB, Castanheira FV, Gozzi A, Czaikoski PG, Niedbala W, Borges M de C, Zamboni DS, Liew FY, Cunha F de Q, Alves Filho JCF. IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population [Internet]. Nature Communications. 2017 ; 8[citado 2024 out. 05 ] Available from: https://doi.org/10.1038/ncomms14919 -
Vancouver
Nascimento DC, Melo PH, Piñeros AR, Ferreira RG, Colón DF, Donate PB, Castanheira FV, Gozzi A, Czaikoski PG, Niedbala W, Borges M de C, Zamboni DS, Liew FY, Cunha F de Q, Alves Filho JCF. IL-33 contributes to sepsis-induced long-term immunosuppression by expanding the regulatory T cell population [Internet]. Nature Communications. 2017 ; 8[citado 2024 out. 05 ] Available from: https://doi.org/10.1038/ncomms14919 - Legionella longbeachae is immunologically silent and highly virulent in vivo
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- MyD88-, but not Nod1- and/or Nod2-deficient mice, show increased susceptibility to polymicrobial sepsis due to impaired local inflammatory response
- Chronic toxoplasma gondii infection exacerbates secondary polymicrobial sepsis
- Mechanism of virulence in the murine moldel of legionella longbeachae infection
- The pattern recognition receptors Nod1 and Nod2 account for neutrophil recruitment to the lungs of mice infected with Legionella pneumophila
- Unraveling the pathogenesis of Legionella longbeachae infection: a role of type IV secretion system to induce mice lethality via pulmonary inflammation
- Regulation of type 17 helper T-cell function by nitric oxide during inflammation
- Interleukin-10 rs2227307 and CXCR2 rs1126579 polymorphisms modulate the predisposition to septic shock
- IL-33 signaling is essential to attenuate viral-induced encephalitis development by downregulating iNOS expression in the central nervous system
Informações sobre o DOI: 10.1038/ncomms14919 (Fonte: oaDOI API)
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