Martin, J.C.J. et al. (2014) Interleukin-22 binding protein (IL-22BP) is constitutively expressed by a subset of conventional dendritic cells and is strongly induced by retinoic acid. Mucosal Immunology, 7(1), pp. 101-113. (doi: 10.1038/mi.2013.28)
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Abstract
Interleukin-22 (IL-22) is mainly produced at barrier surfaces by T cells and innate lymphoid cells and is crucial to maintain epithelial integrity. However, dysregulated IL-22 action leads to deleterious inflammation and is involved in diseases such as psoriasis, intestinal inflammation, and cancer. IL-22 binding protein (IL-22BP) is a soluble inhibitory IL-22 receptor and may represent a crucial regulator of IL-22. We show both in rats and mice that, in the steady state, the main source of IL-22BP is constituted by a subset of conventional dendritic cells (DCs) in lymphoid and non-lymphoid tissues. In mouse intestine, IL-22BP was specifically expressed in lamina propria CD103+CD11b+ DC. In humans, IL-22BP was expressed in immature monocyte-derived DC and strongly induced by retinoic acid but dramatically reduced upon maturation. Our data suggest that a subset of immature DCs may actively participate in the regulation of IL-22 activity in the gut by producing high levels of IL-22BP.
Item Type: | Articles |
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Status: | Published |
Refereed: | Yes |
Glasgow Author(s) Enlighten ID: | Aumeunier, Dr Aude and Milling, Professor Simon and Utriainen, Dr Lotta and Mowat, Professor Allan and Cerovic, Dr Vuk and Houston, Miss Stephanie |
Authors: | Martin, J.C.J., Bériou, G., Heslan, M., Chauvin, C., Utriainen, L., Aumeunier, A., Scott, C.L., Mowat, A., Cerovic, V., Houston, S.A., Leboeuf, M., Hubert, F.X., Hémont, C., Merad, M., Milling, S., and Josien, R. |
College/School: | College of Medical Veterinary and Life Sciences > School of Infection & Immunity College of Medical Veterinary and Life Sciences College of Medical Veterinary and Life Sciences > School of Infection & Immunity > Centre for Virus Research |
Journal Name: | Mucosal Immunology |
ISSN: | 1933-0219 |
ISSN (Online): | 1935-3456 |
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