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

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HAL Id: inserm-00643975

https://www.hal.inserm.fr/inserm-00643975

Submitted on 23 Nov 2011

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A subset of dendritic cells as a major and constitutive

source of IL-22BP

Jérôme Martin, Gaelle Bériou, Michèle Heslan, Céline Bossard, Anne-Chantal

Knol, Brigitte Dréno, Simon Milling, Miriam Merad, Régis Josien

To cite this version:

Jérôme Martin, Gaelle Bériou, Michèle Heslan, Céline Bossard, Anne-Chantal Knol, et al.. A subset

of dendritic cells as a major and constitutive source of IL-22BP. 6th european workshop on

immune-mediated inflammatory diseases, Nice, France. pp.P2. �inserm-00643975�

(2)

P O S T E R P R E S E N T A T I O N

Open Access

A subset of dendritic cells as a major and

constitutive source of IL-22BP

Jérôme Martin

1,2

, Gaelle Bériou

1

, Michèle Heslan

1

, Céline Bossard

3

, Anne-Chantal Knol

4

, Brigitte Dréno

4

,

Simon Milling

5

, Miriam Merad

6

, Régis Josien

1,2*

From 6th European Workshop on Immune-Mediated Inflammatory Diseases

Nice, France. 23-25 November 2011

Introduction

IL-22 is a cytokine produced by T cells and innate lym-phocytes. 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.

Aims

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

Methods

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.

Results

IL-22BP mRNA was expressed at high levels in rat second-ary 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 expres-sion 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, immu-nostaining experiments identified stellate IL-22BP+cells in

colon lamina propria and dermis. In vitro, IL-22BP expres-sion was induced during MDDC differentiation and reti-noic 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.

Conclusion

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.

Author details

1INSERM U643, ITUN, Nantes, France.2Laboratoire d’Immunologie, Nantes, France.3Service d’Anatomo-Pathologie, Nantes, France.4INSERM U892, Laboratoire d’Immuno-Dermatologie, CHU Nantes, Nantes, France.5University of Glasgow, Glasgow, UK.6Mount Sinai School of Medicine, New York, USA. Published: 23 November 2011

doi:10.1186/1479-5876-9-S2-P2

Cite this article as: Martin et al.: A subset of dendritic cells as a major and constitutive source of IL-22BP. Journal of Translational Medicine 2011 9(Suppl 2):P2.

1INSERM U643, ITUN, Nantes, France

Full list of author information is available at the end of the article Martin et al. Journal of Translational Medicine 2011, 9(Suppl 2):P2 http://www.translational-medicine.com/content/9/S2/P2

© 2011 Martin et al; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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