Renate Effner, Germany

Chair and Institute of Environmental Medicine, UNIKA-T Technical University of Munich and Helmholtz Zentrum München - German Research Center for Environmental Health

Presenter Of 1 Presentation

Poster Display T Cell Biology

EPITHELIAL IMMUNE RESPONSES ON MICROBIOBAL AND ENVIRONMENTAL TRIGGERS IN STAT1/STAT3 IMBALANCED PRIMARY IMMUNODEFICIENCIES

Lecture Time
10:05 - 10:06
Room
Poster Area
Date
19.09.2019, Thursday
Session Time
10:00 - 17:00
Board Number
163
Presentation Topic
T Cell Biology

Abstract

Background and Aims

Patients with STAT1/STAT3 imbalanced primary immunodeficiencies frequently suffer from chronic microbial skin and respiratory infections caused by a compromised Th17 immunity. The environmental sensor aryl hydrocarbon receptor (AHR) has immune-modulating functions by interfering with Th17 immunity, with potential beneficial effect in STAT‑imbalanced patients. Here, we assess the effect of Th17 immunity and AHR pathway on microbiobal challenges in STAT-imbalanced patients.

Methods

Activated human peripheral blood mononuclear cells of healthy subjects and STAT-imbalanced patients were assessed for the expression of AHR pathway related targets and Th17 cytokines upon treatment with AHR agonists. Responses of human epithelial cells to environmental signals in combination with STAT1/STAT3 activating cytokines were analyzed regarding the production of antimicrobial peptides and pro-inflammatory mediators.

Results

AHR activation increased the Th17 cytokine IL-22 and AHR pathway related genes in PBMCs of healthy subjects and STAT-imbalanced patients. Despite the increase, IL-22 concentration in patients do not reach the level found in healthy subjects. Challenge of epithelial cells by environmental triggers increased the production of antimicrobial peptides whereas pro-inflammatory chemokines were reduced.

Conclusions

The observed induction of IL-22 in STAT-imbalanced patients by environmentally-triggered AHR signaling changed Th17 immunity with possible beneficial effects of an increased epithelial defense.

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