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Immunity. 2015 Jul 21;43(1):29-40. doi: 10.1016/j.immuni.2015.07.007.

Barrier Epithelial Cells and the Control of Type 2 Immunity.

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1
VIB Inflammation Research Center, Technologiepark 927, 9052 Ghent, Belgium; Laboratory of Immunoregulation and Mucosal Immunology, Department of Respiratory Medicine, Ghent University, De Pintelaan 185, 9000 Ghent, Belgium. Electronic address: hamida.hammad@irc.vib-ugent.be.
2
VIB Inflammation Research Center, Technologiepark 927, 9052 Ghent, Belgium; Laboratory of Immunoregulation and Mucosal Immunology, Department of Respiratory Medicine, Ghent University, De Pintelaan 185, 9000 Ghent, Belgium; Department of Pulmonary Medicine, ErasmusMC, Dr Molewaterplein 50, 3015 GE Rotterdam, the Netherlands. Electronic address: bart.lambrecht@irc.vib-ugent.be.

Abstract

Type-2-cell-mediated immunity, rich in eosinophils, basophils, mast cells, CD4(+) T helper 2 (Th2) cells, and type 2 innate lymphoid cells (ILC2s), protects the host from helminth infection but also drives chronic allergic diseases like asthma and atopic dermatitis. Barrier epithelial cells (ECs) represent the very first line of defense and express pattern recognition receptors to recognize type-2-cell-mediated immune insults like proteolytic allergens or helminths. These ECs mount a prototypical response made up of chemokines, innate cytokines such as interleukin-1 (IL-1), IL-25, IL-33, and thymic stromal lymphopoietin (TSLP), as well as the alarmins uric acid, ATP, HMGB1, and S100 proteins. These signals program dendritic cells (DCs) to mount Th2-cell-mediated immunity and in so doing boost ILC2, basophil, and mast cell function. Here we review the general mechanisms of how different stimuli trigger type-2-cell-mediated immunity at mucosal barriers and how this leads to protection or disease.

PMID:
26200011
DOI:
10.1016/j.immuni.2015.07.007
[Indexed for MEDLINE]
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