Dendritic cells and the pathogenesis of rheumatoid arthritis

Thomas, R., MacDonald, K. P. A., Pettit, A. R., Cavanagh, L. L., Padmanabha, J. and Zehntner, S. (1999) Dendritic cells and the pathogenesis of rheumatoid arthritis. Journal of Leukocyte Biology, 66 2: 286-292.


Author Thomas, R.
MacDonald, K. P. A.
Pettit, A. R.
Cavanagh, L. L.
Padmanabha, J.
Zehntner, S.
Title Dendritic cells and the pathogenesis of rheumatoid arthritis
Journal name Journal of Leukocyte Biology   Check publisher's open access policy
ISSN 0741-5400
Publication date 1999-08-01
Sub-type Article (original research)
Volume 66
Issue 2
Start page 286
End page 292
Total pages 7
Place of publication Bethesda, USA
Publisher Society for Leukocyte Biology
Language eng
Subject C1
730114 Skeletal system and disorders (incl. arthritis)
1107 Immunology
110322 Rheumatology and Arthritis
Abstract Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease in which unknown arthrogenic autoantigen is presented to CD4(+) T cells. The strong association of the disease with an epitope within the HLA-DR chain shared between various alleles of HLA-DR4 and DR1 emphasizes the importance of antigen presentation. This immune response predominantly occurs in the synovial tissue and fluid of the joints and autoreactive T cells are readily demonstrable in both the synovial compartment and blood. Circulating dendritic cells (DC) are phenotypically and functionally identical with normal peripheral blood (PB) DC. In the synovial tissue, fully differentiated perivascular DC are found in close association with T cells and with B cell follicles, sometimes containing follicular DC. These perivascular DC migrate across the activated endothelium from blood and receive differentiative signals within the joint from monocyte-derived cytokines and CD40-ligand(+) T cells. In the SF, DC manifest an intermediate phenotype, similar to that of monocyte-derived DC in vitro. Like a delayed-type hypersensitivity response, the rheumatoid synovium represents an effector site. DC at many effector sites have a characteristic pattern of infiltration and differentiation. It is important to note that the effector response is not self-limiting in RA autoimmune inflammation. In this article, we argue that the presentation of self-antigen by DC and by autoantibody-producing B cells is critical for the perpetuation of the autoimmune response. Permanently arresting this ongoing immune response with either pharmaceutical agents or immunotherapy is a major challenge for immunology.
Keyword Cell Biology
Hematology
Immunology
Autoimmune Response
Immunotherapy
Synovial Fluid
Synovial Tissue
Collagen-induced Arthritis
Mixed Leukocyte Reactions
Necrosis-factor-alpha
Intercellular-adhesion Molecule-1
Peripheral-blood Lymphocytes
Anti-cd4 Monoclonal-antibody
Colony-stimulating Factor
Synovial-fluid
T-cells
Mononuclear-cells
Q-Index Code C1

Document type: Journal Article
Sub-type: Article (original research)
Collection: UQ Diamantina Institute Publications
 
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Created: Wed, 11 Jun 2008, 01:22:44 EST