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Eosinophils from eosinophilic oesophagitis patients have T cell suppressive capacity and express FOXP3

Authors :
Robert Saalman
M Bove
A Welin
Christine Lingblom
Christine Wennerås
Madeleine Ingelsten
J Wallander
Henrik Bergquist
Source :
Clinical and Experimental Immunology. 187:455-465
Publication Year :
2016
Publisher :
Oxford University Press (OUP), 2016.

Abstract

Summary Eosinophilic esophagitis (EoE) is an antigen-driven T cell-mediated chronic inflammatory disease where food and environmental antigens are thought to have a role. Human eosinophils express the immunoregulatory protein galectin-10 and have T cell suppressive capacity similar to regulatory T cells (Tregs). We hypothesized that one function of eosinophils in EoE might be to regulate the T cell-driven inflammation in the oesophagus. This was tested by evaluating the suppressive capacity of eosinophils isolated from the blood of adult EoE patients in a mixed lymphocyte reaction. In addition, eosinophilic expression of forkhead box protein 3 (FOXP3), the canonical transcription factor of Tregs, was determined by conventional and imaging flow cytometry, quantitative polymerase chain reaction (qPCR), confocal microscopy and immunoblotting. It was found that blood eosinophils from EoE patients had T cell suppressive capacity, and that a fraction of the eosinophils expressed FOXP3. A comparison of EoE eosinophils with healthy control eosinophils indicated that the patients' eosinophils had inferior suppressive capacity. Furthermore, a higher percentage of the EoE eosinophils expressed FOXP3 protein compared with the healthy eosinophils, and they also had higher FOXP3 protein and mRNA levels. FOXP3 was found in the cytosol and nucleus of the eosinophils from both the patients and healthy individuals, contrasting with the strict nuclear localization of FOXP3 in Tregs. To conclude, these findings suggest that the immunoregulatory function of eosinophils may be impaired in EoE.

Details

ISSN :
13652249 and 00099104
Volume :
187
Database :
OpenAIRE
Journal :
Clinical and Experimental Immunology
Accession number :
edsair.doi.dedup.....0af9407cf2b4595d91170f15c344b038
Full Text :
https://doi.org/10.1111/cei.12898