Loss of IL-22 inhibits autoantibody formation in collagen-induced arthritis in mice

Autor: PS Asmawidjaja, Jurre Y. Siegers, Rada Amin, Tom Cupedo, Frédéric Mourcin, Jan Piet van Hamburg, Karin Tarte, Adriana M.C. Mus, Rudi W. Hendriks, Odilia B. J. Corneth, Natalie Papazian, E Lubberts, Rogier M. Reijmers
Přispěvatelé: Erasmus University Medical Center [Rotterdam] (Erasmus MC), Microenvironnement et cancer (MiCa), Université de Rennes (UR)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Etablissement Français du Sang Bretagne, EFS, Service d’immunologie, de thérapie cellulaire et d’hématopoïèse, Hôpital Pontchaillou, Dutch Arthritis Foundation. Grant Number: 0801043, Netherlands Organization for Scientific Research. Grant Numbers: 917.10.377, 916.13.011, Human Frontier Science Program. Grant Number: RGP0006/2009, Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Jonchère, Laurent, Pathology, Clinical Immunology and Rheumatology, Pulmonary Medicine, Rheumatology, Hematology
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
medicine.medical_treatment
Arthritis
Lymphocyte Activation
Severity of Illness Index
Arthritis
Rheumatoid
Mice
0302 clinical medicine
Antibody Specificity
Immunology and Allergy
Cells
Cultured
Mice
Knockout
[SDV.MHEP.RSOA] Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system
B cell
Interleukin
3. Good health
Cytokine
medicine.anatomical_structure
Autoantibody formation
[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal system
[SDV.IMM]Life Sciences [q-bio]/Immunology
Chemokines
Stromal cell
[SDV.IMM] Life Sciences [q-bio]/Immunology
Immunology
Plasma Cells
Biology
03 medical and health sciences
SDG 3 - Good Health and Well-being
medicine
Animals
CXCL13
Rheumatoid arthritis
Autoantibodies
Interleukins
Autoantibody
Germinal center
Receptors
Interleukin
medicine.disease
Arthritis
Experimental
Coculture Techniques
Disease Models
Animal
030104 developmental biology
Antibody Formation
Th17 Cells
Interleukin 22 (IL-22)
Stromal Cells
030215 immunology
Zdroj: European Journal of Immunology
European Journal of Immunology, 2016, 46 (6), pp.1404-1414. ⟨10.1002/eji.201546241⟩
European Journal of Immunology, Wiley-VCH Verlag, 2016, 46 (6), pp.1404-1414. ⟨10.1002/eji.201546241⟩
European journal of immunology, 46(6), 1404-1414. Wiley-VCH Verlag
European Journal of Immunology, 46(6), 1404-1414. Wiley-VCH
ISSN: 0014-2980
1521-4141
DOI: 10.1002/eji.201546241
Popis: International audience; Interleukin 22 (IL-22) expression is associated with increased joint destruction and disease progression in rheumatoid arthritis (RA). Although IL-22 is considered a pro-inflammatory cytokine, its mechanism of action in RA remains incompletely understood. Here, we used the collagen-induced arthritis model in IL-22 deficient (IL-22(-/-) ) mice to study the role of IL-22 in RA. In spite of normal disease incidence, disease severity is significantly diminished in IL-22(-/-) mice. Moreover, pathogenicity of Th17 cells and development and function of B cells are unaffected. In contrast, splenic plasma cells, as well as serum autoantibody titers, are reduced in the absence of IL-22. At the peak of disease, germinal centers (GCs) are severely reduced in the spleens of IL-22(-/-) mice, correlating with a decline in GC B-cell numbers. Within the GC, we identified IL-22R1 expressing follicular dendritic cell-like stromal cells. Human lymphoid stromal cells respond to IL-22 ex vivo by inducing transcription of CXCL12 and CXCL13. We therefore postulate IL-22 as an important enhancer of the GC reaction, maintaining chemokine levels for the persistence of GC reactions, essential for the production of autoantibody-secreting plasma cells. Blocking IL-22 might therefore prevent immune-complex deposition and destruction of joints in RA patients.
Databáze: OpenAIRE
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