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Manipulation of Autophagy by Bacterial Pathogens Impacts Host Immunity.
Kunz, Tobias C; Viana, Flávia; Buchrieser, Carmen; Escoll, Pedro.
Afiliação
  • Kunz TC; Institut Pasteur, Biologie des Bactéries Intracellulaires, Paris, France, and CNRS UMR 3525, Paris, France.
  • Viana F; Institut Pasteur, Biologie des Bactéries Intracellulaires, Paris, France, and CNRS UMR 3525, Paris, France.
  • Buchrieser C; Institut Pasteur, Biologie des Bactéries Intracellulaires, Paris, France, and CNRS UMR 3525, Paris, France.
  • Escoll P; Institut Pasteur, Biologie des Bactéries Intracellulaires, Paris, France, and CNRS UMR 3525, Paris, France.
Curr Issues Mol Biol ; 25: 81-98, 2018.
Article em En | MEDLINE | ID: mdl-28875941
Autophagy is a highly conserved catabolic process, degrading unnecessary or damaged components in the eukaryotic cell to maintain cellular homeostasis, but it is also an intrinsic cellular defence mechanism to remove invading pathogens. A crosstalk between autophagy and innate or adaptive immune responses has been recently reported, whereby autophagy influences both, innate and adaptive immunity like the production and secretion of pro-inflammatory cytokines or MHC class II antigen presentation to T cells. Pathogenic bacteria have evolved diverse strategies to manipulate autophagy, mechanisms that also impact host immune responses at different levels. Here we discuss the influence of autophagy on self-autonomous, innate and adaptive immunity and then focus on how bacterial mechanisms that shape autophagy may impact the host immune system.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Autofagia / Linfócitos T / Interações Hospedeiro-Patógeno / Bactérias Gram-Negativas / Bactérias Gram-Positivas / Imunidade Inata Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Autofagia / Linfócitos T / Interações Hospedeiro-Patógeno / Bactérias Gram-Negativas / Bactérias Gram-Positivas / Imunidade Inata Idioma: En Ano de publicação: 2018 Tipo de documento: Article