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A pathogenic role for the integrin CD103 in experimental allergic airways disease

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posted on 2023-05-18, 23:42 authored by Fear, VS, Lai, SP, Graeme ZoskyGraeme Zosky, Perks, KL, Gorman, S, Blank, F, von Garnier, C, Stumbles, PA, Strickland, DH
The integrin CD103 is the aE chain of integrin aEb7 that is important in the maintenance of intraepithelial lymphocytes and recruitment of T cells and dendritic cells (DC) to mucosal surfaces. The role of CD103 in intestinal immune homeostasis has been well described, however, its role in allergic airway inflammation is less well understood. In this study, we used an ovalbumin (OVA)-induced, CD103-knockout (KO) BALB/c mouse model of experimental allergic airways disease (EAAD) to investigate the role of CD103 in disease expression, CD4+ T-cell activation and DC activation and function in airways and lymph nodes. We found reduced airways hyper-responsiveness and eosinophil recruitment to airways after aerosol challenge of CD103 KO compared to wild-type (WT) mice, although CD103 KO mice showed enhanced serum OVA-specific IgE levels. Following aerosol challenge, total numbers of effector and regulatory CD4+ T-cell subsets were significantly increased in the airways of WT but not CD103 KO mice, as well as a lack of DC recruitment into the airways in the absence of CD103. While total airway DC numbers, and their in vivo allergen capture activity, were essentially normal in steady-state CD103 KO mice, migration of allergen-laden airway DC to draining lymph nodes was disrupted in the absence of CD103 at 24 h after aerosol challenge. These data support a role for CD103 in the pathogenesis of EAAD in BALB/c mice through local control of CD4+ T cell and DC subset recruitment to, and migration from, the airway mucosa during induction of allergic inflammation.

History

Publication title

Physiological Reports

Volume

4

Issue

21

Article number

e13021

Number

e13021

Pagination

1-13

ISSN

2051-817X

Department/School

Tasmanian School of Medicine

Publisher

John Wiley & Sons Ltd.

Place of publication

United Kingdom

Rights statement

Copyright 2016 The Authors. Physiological Reports Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/

Repository Status

  • Open

Socio-economic Objectives

Clinical health not elsewhere classified

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