| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Brouwers, Conny Boross, Peter Verbeek, J. Sjef Asmawidjaja, Patrick Ramirez, Javier Martin Van Der Kaa, Jos Claassens, Jill W. C. Lubberts, Erik Yilmaz-Elis, A. Seda Brem, Maarten D. Mangsbo, Sara M. Breukel, Cor Mus, Anne-Marie |
| Description |
Author Affiliation: Yilmaz-Elis AS ( Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands); Ramirez JM ( Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands); Asmawidjaja P ( Department of Rheumatology, Erasmus MC, University Medical Center, 3000 CA Rotterdam, The Netherlands); van der Kaa J ( Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands); Mus AM ( Department of Rheumatology, Erasmus MC, University Medical Center, 3000 CA Rotterdam, The Netherlands); Brem MD ( Department of Rheumatology, Erasmus MC, University Medical Center, 3000 CA Rotterdam, The Netherlands); Claassens JW ( Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands); Breukel C ( Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands); Brouwers C ( Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands); Mangsbo SM ( Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands.); Boross P ( Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands); Lubberts E ( Department of Rheumatology, Erasmus MC, University Medical Center, 3000 CA Rotterdam, The Netherlands); Verbeek JS ( Department of Human Genetics, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands) |
| Abstract |
Extensive analysis of a variety of arthritis models in germline KO mice has revealed that all four receptors for the Fc part of IgG (FcγR) play a role in the disease process. However, their precise cell type-specific contribution is still unclear. In this study, we analyzed the specific role of the inhibiting FcγRIIb on B lymphocytes (using CD19Cre mice) and in the myeloid cell compartment (using C/EBP Cre mice) in the development of arthritis induced by immunization with either bovine or chicken collagen type II. Despite their comparable anti-mouse collagen autoantibody titers, full FcγRIIb knockout (KO), but not B cell-specific FcγRIIb KO, mice showed a significantly increased incidence and severity of disease compared with wild-type control mice when immunized with bovine collagen. When immunized with chicken collagen, disease incidence was significantly increased in pan-myeloid and full FcγRIIb KO mice, but not in B cell-specific KO mice, whereas disease severity was only significantly increased in full FcγRIIb KO mice compared with incidence and severity in wild-type control mice. We conclude that, although anti-mouse collagen autoantibodies are a prerequisite for the development of collagen-induced arthritis, their presence is insufficient for disease development. FcγRIIb on myeloid effector cells, as a modulator of the threshold for downstream Ab effector pathways, plays a dominant role in the susceptibility to collagen-induced arthritis, whereas FcγRIIb on B cells, as a regulator of Ab production, has a minor effect on disease susceptibility. |
| ISSN |
00221767 |
| e-ISSN |
15506606 |
| Journal |
The Journal of Immunology |
| Issue Number |
12 |
| Volume Number |
192 |
| Language |
English |
| Publisher |
The American Association of Immunologists |
| Publisher Date |
2014-06-15 |
| Publisher Place |
United States |
| Access Restriction |
Open |
| Subject Keyword |
Arthritis, Experimental Immunology Autoantibodies B-lymphocytes Myeloid Cells Receptors, Igg Animals Genetics Pathology Collagen Type Ii Mice Mice, Knockout Organ Specificity Research Support, Non-u.s. Gov't Discipline Immunology |
| Content Type |
Text |
| Resource Type |
Article |
| Subject |
Immunology and Allergy Immunology |
