ICOS regulates the pool of group 2 innate lymphoid cells under homeostatic and inflammatory conditions in mice. Issue 10 (31st August 2015)

• Record Type: Journal Article
• Authors: Paclik, Daniela; Stehle, Christina; Lahmann, Annette; Hutloff, Andreas; Romagnani, Chiara
• Is Part Of: European journal of immunology. Volume 45:Issue 10(2015:Oct.)
• Page Start: 2766
• Page End: 2772
• Publication Date: 2015-08-31
• Subjects: Immunology -- Periodicals; 616.079
• DOI: 10.1002/eji.201545635
• Languages: English
• ISSNs: 0014-2980

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Group 2 innate lymphoid cells (ILC2s) are innate effectors playing an important role in the defense against helminthic infections and in the pathogenesis of allergic inflammation. Cytokines have been identified as the major stimuli driving ILC2 activation and expansion. Conversely, it is unclear whether costimulatory molecules contribute to regulation of ILC2 functions. ILC2s display high expression of inducible T‐cell costimulator (ICOS), which belongs to the CD28 superfamily, and which has been shown to control late effector T‐cell functions, and is of utmost importance for the humoral immune response. However, the biological function of ICOS expression on ILC2s is unknown. Here, we show that ICOS signaling in mice regulates ILC2 homeostasis independently of T cells and B cells, by promoting proliferation and accumulation of mature ILC2s in lung and intestine. In a model of IL‐33‐induced airway inflammation, ICOS controls ILC2 activation and eosinophil infiltration in the lung. Our data identify a role of ICOS in innate immunity and indicate that not only cytokines, but also costimulatory pathways such as those involving ICOS, can contribute to regulate the ILC2 pool. Thus, ICOS costimulation blockade, which is currently under clinical evaluation for inhibiting the humoral immune response, could also target innate inflammatory circuits.</p> </abstract>