6 research outputs found

    Proviral changes in the autophagy status of infected cells differentially affect the outcome of secondary bacterial infection at the cellular level.

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    (A) A simplified representation of the ordered steps that constitute the autophagy flux (see main text) (AR: autophagy receptors). (B) Summary of available observations on the outcome of secondary bacterial infection of measles virus-infected epithelial cells (Salmonella Typhimurium or Shigella flexneri) or HIV-1-infected macrophages (Mycobacterium tuberculosis).</p

    Autophagie et co-infection

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    International audienceAutophagy is a highly conserved process that utilizes lysosomes to selectively degrade a variety of intracellular cargo, thus providing quality control over cellular components and maintaining cellular regulatory functions. Autophagy is triggered by multiple stimuli ranging from nutrient starvation to microbial infection. Autophagy extensively shapes and modulates the inflammatory response, the concerted action of immune cells, and secreted mediators aimed to eradicate a microbial infection or to heal sterile tissue damage. Here, we first review how autophagy affects innate immune signaling, cell-autonomous immune defense, and adaptive immunity. Then, we discuss the role of non- canonical autophagy in context of microbial infections and inflammation. Finally, we review how crosstalk between autophagy and inflammation influ-ences infectious diseases as well as metabolic and autoimmune disorders
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