Death Receptor 3 regulates distinct pathological attributes of acute versus chronic murine allergic lung inflammation.

Autor: Singh RK; Division of Infection & Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK., Perks WV; Division of Infection & Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK., Twohig JP; Division of Infection & Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK., Kidd EJ; School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Cardiff CF10 3NB, UK., Broadley K; School of Pharmacy and Pharmaceutical Sciences, Cardiff University, Cardiff CF10 3NB, UK., Farrow SN; CRT discoveries laboratories, Babraham Research Campus, Cambridge CB22 3AT, UK., Williams AS; Division of Infection & Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK., Taylor PR; Division of Infection & Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK., Wang ECY; Division of Infection & Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK. Electronic address: wangec@cf.ac.uk.
Jazyk: angličtina
Zdroj: Cellular immunology [Cell Immunol] 2017 Oct; Vol. 320, pp. 62-70. Date of Electronic Publication: 2017 Sep 15.
DOI: 10.1016/j.cellimm.2017.09.005
Abstrakt: The Death Receptor 3 (DR3)/Tumour Necrosis Factor-like cytokine 1A (TL1A) axis stimulates effector T cells and type 2 innate lymphocytes (ILC2) that trigger cytokine release and drive disease pathology in several inflammatory and autoimmune diseases, including murine models of acute allergic lung inflammation (ALI). The aim of this study was to elucidate the role of DR3 in chronic ALI compared to acute ALI, using mice genetically deficient in the DR3 gene (DR3 ko ). Results showed DR3 expression in the lungs of wild-type mice was up-regulated following induction of acute ALI and this increased expression was maintained in chronic disease. DR3 ko mice were resistant to cellular accumulation within the alveolar passages in acute, but not chronic ALI. However, DR3 ko mice displayed reduced immuno-histopathology and goblet cell hyperplasia; hallmarks of the asthmatic phenotype; in chronic, but not acute ALI. These data suggest DR3 is a potential therapeutic target, involved in temporally distinct aspects of ALI progression and pathogenesis.
(Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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