Eosinophils suppress Th1 responses and restrict bacterially induced gastrointestinal inflammation.

Arnold, Isabelle C; Artola-Borán, Mariela; Tallón de Lara, Paulino; Kyburz, Andreas; Taube, Christian; Ottemann, Karen; van den Broek, Maries; Yousefi, Shida; Simon, Hans-Uwe; Müller, Anne (2018). Eosinophils suppress Th1 responses and restrict bacterially induced gastrointestinal inflammation. Journal of experimental medicine, 215(8), pp. 2055-2072. Rockefeller University Press 10.1084/jem.20172049

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Eosinophils are predominantly known for their contribution to allergy. Here, we have examined the function and regulation of gastrointestinal eosinophils in the steady-state and during infection with or We find that eosinophils are recruited to sites of infection, directly encounter live bacteria, and activate a signature transcriptional program; this applies also to human gastrointestinal eosinophils in humanized mice. The genetic or anti-IL-5-mediated depletion of eosinophils results in improved control of the infection, increased inflammation, and more pronounced Th1 responses. Eosinophils control Th1 responses via the IFN-γ-dependent up-regulation of PD-L1. Furthermore, we find that the conditional loss of IFN-γR in eosinophils phenocopies the effects of eosinophil depletion. Eosinophils further possess bactericidal properties that require their degranulation and the deployment of extracellular traps. Our results highlight two novel functions of this elusive cell type and link it to gastrointestinal homeostasis and anti-bacterial defense.

Item Type:

Journal Article (Original Article)

Division/Institute:

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

UniBE Contributor:

Yousefi, Shida and Simon, Hans-Uwe

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1540-9538

Publisher:

Rockefeller University Press

Language:

English

Submitter:

Jana Berger

Date Deposited:

10 Jul 2018 08:52

Last Modified:

23 Oct 2019 14:06

Publisher DOI:

10.1084/jem.20172049

PubMed ID:

29970473

BORIS DOI:

10.7892/boris.118387

URI:

https://boris.unibe.ch/id/eprint/118387

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