Regulation of the innate immune system by autophagy: neutrophils, eosinophils, mast cells, NK cells.

Germic, Nina; Frangez, Ziva; Yousefi, Shida; Simon, Hans-Uwe (2019). Regulation of the innate immune system by autophagy: neutrophils, eosinophils, mast cells, NK cells. Cell death and differentiation, 26(4), pp. 703-714. Nature Publishing Group 10.1038/s41418-019-0295-8

[img] Text
Simon_Regulation of the innate immune system...NK cells.pdf - Published Version
Restricted to registered users only
Available under License Publisher holds Copyright.

Download (1MB) | Request a copy

Autophagy is an evolutionally conserved, highly regulated catabolic process that combines cellular functions required for the regulation of metabolic balance under conditions of stress with those needed for the degradation of damaged cell organelles via the lysosomal machinery. The importance of autophagy for cell homeostasis and survival has long been appreciated. Recent data suggest that autophagy is also involved in non-metabolic functions that impact the immune system. Here, we reflect in two review articles the recent literature pointing to an important role for autophagy in innate immune cells. In this article, we focus on neutrophils, eosinophils, mast cells, and natural killer cells. We mainly discuss the influence of autophagy on functional cellular responses and its importance for overall host defense. In the companion review, we present the role of autophagy in the functions performed by monocytes/macrophages and dendritic cells.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology

Graduate School:

Graduate School for Cellular and Biomedical Sciences (GCB)

UniBE Contributor:

Germic, Nina, Frangez, Ziva, Yousefi, Shida, Simon, Hans-Uwe

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1350-9047

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Celine Joray

Date Deposited:

15 May 2019 14:30

Last Modified:

05 Dec 2022 15:27

Publisher DOI:

10.1038/s41418-019-0295-8

PubMed ID:

30737478

BORIS DOI:

10.7892/boris.127436

URI:

https://boris.unibe.ch/id/eprint/127436

Actions (login required)

Edit item Edit item
Provide Feedback