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A subset of dendritic cells as a major and constitutive source of IL-22BP

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Journal of Translational Medicine20119 (Suppl 2) :P2

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  • Psoriasis
  • Retinoic Acid
  • Retinoic Acid Receptor
  • Crohn Disease
  • Cellular Source


IL-22 is a cytokine produced by T cells and innate lymphocytes. Its receptor is exclusively expressed by non hematopoietic cells mostly epithelial cells and hepatocytes. IL-22 has pathogenic or protective effects depending on the model. A role for IL-22 is suggested in IMID such as psoriasis, rheumatoid arthritis and Crohn disease. IL-22BP is a soluble inhibitory receptor specific for IL-22 whose cellular source and physiological role are mainly unknown.


To identify the cellular source of IL-22BP in vivo and its regulation of expression.


Rat dendritic cells (DCs) were prepared from spleen. Human DCs were derived from monocytes (MDDC) in the presence of GM-CSF+IL-4. IL-22BP mRNA expression was assessed by q-PCR. Immunostaining experiments were performed with polyclonal and/or monoclonal Ab to IL-22BP. IL-22BP in serum was identified by WB.


IL-22BP mRNA was expressed at high levels in rat secondary lymphoid organs and intestine. In spleen, IL-22BP mRNA was restricted to a CD4+SIRPA+ subset of DCs. This expression was constitutive. Similar results were obtained in lymph nodes. IL-22BP expression in DCs was confirmed at the protein level. An even stronger expression was found in a subset of lymph DCs migrating from gut. In mouse, IL-22BP expression appeared restricted to the CD103+ subsets of intestine DCs. In human, immunostaining experiments identified stellate IL-22BP+ cells in colon lamina propria and dermis. In vitro, IL-22BP expression was induced during MDDC differentiation and retinoic acid receptor alpha agonist dramatically enhanced this expression. IL-22BP expression was rapidly down-regulated following maturation both in rat and human DC. Finally, WB analysis revealed high levels of serum IL-22BP in healthy volunteers.


These results indicate that tissue and lymphoid DCs are a main source of IL-22BP suggesting a role for these DCs in regulating IL-22 at epithelial barriers.

Authors’ Affiliations

INSERM U643, ITUN, Nantes, France
Laboratoire d’Immunologie, Nantes, France
Service d’Anatomo-Pathologie, Nantes, France
INSERM U892, Laboratoire d’Immuno-Dermatologie, CHU Nantes, Nantes, France
University of Glasgow, Glasgow, UK
Mount Sinai School of Medicine, New York, USA


© Martin et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.