Regulation of eosinophil functions by autophagy.

Germic, Nina; Hosseini, Aref; Yousefi, Shida; Karaulov, Alexander; Simon, Hans-Uwe (2021). Regulation of eosinophil functions by autophagy. Seminars in immunopathology, 43(3), pp. 347-362. Springer 10.1007/s00281-021-00860-1

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Eosinophils are granule-containing leukocytes which develop in the bone marrow. For many years, eosinophils have been recognized as cytotoxic effector cells, but recent studies suggest that they perform additional immunomodulatory and homeostatic functions. Autophagy is a conserved intracellular process which preserves cellular homeostasis. Autophagy defects have been linked to the pathogenesis of many human disorders. Evidence for abnormal regulation of autophagy, including decreased or increased expression of autophagy-related (ATG) proteins, has been reported in several eosinophilic inflammatory disorders, such as Crohn's disease, bronchial asthma, eosinophilic esophagitis, and chronic rhinosinusitis. Despite the increasing extent of research using preclinical models of immune cell-specific autophagy deficiency, the physiological relevance of autophagic pathway in eosinophils has remained unknown until recently. Owing to the increasing evidence that eosinophils play a role in keeping organismal homeostasis, the regulation of eosinophil functions is of considerable interest. Here, we discuss the most recent advances on the role of autophagy in eosinophils, placing particular emphasis on insights obtained in mouse models of infections and malignant diseases in which autophagy has genetically dismantled in the eosinophil lineage. These studies pointed to the possibility that autophagy-deficient eosinophils exaggerate inflammation. Therefore, the pharmacological modulation of the autophagic pathway in these cells could be used for therapeutic interventions.

Item Type:

Journal Article (Review Article)

Division/Institute:

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

UniBE Contributor:

Germic, Nina, Hosseini, Aref, Yousefi, Shida, Simon, Hans-Uwe

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1863-2300

Publisher:

Springer

Language:

English

Submitter:

Celine Joray

Date Deposited:

01 Jul 2021 09:45

Last Modified:

05 Dec 2022 15:51

Publisher DOI:

10.1007/s00281-021-00860-1

PubMed ID:

34019141

Uncontrolled Keywords:

Autophagy Degranulation Differentiation Eosinophil Eosinophilic disease Eosinophilic leukemia

BORIS DOI:

10.48350/157251

URI:

https://boris.unibe.ch/id/eprint/157251

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