[CITATION][C] Synergistic activity of interleukin‐4 and interleukin‐10 in suppression of inflammation and joint destruction in rheumatoid arthritis

JAG van Roon, FPJG Lafeber… - Arthritis & Rheumatism …, 2001 - Wiley Online Library
JAG van Roon, FPJG Lafeber, JWJ Bijlsma
Arthritis & Rheumatism: Official Journal of the American College …, 2001Wiley Online Library
Rheumatoid arthritis (RA) is a disease dominated by joint inflammation, accompanied by
several peripheral inflammatory manifestations (1). Although the etiology of RA is still not
fully understood, the pathogenesis is known to involve chronic synovitis leading to
destruction of joint tissues (in particular, cartilage and bone) and consequently, serious
impairment of joint function (2). Patients also exhibit features of systemic inflammation (such
as marked acute-phase responses), and the disease is associated with autoimmune …
Rheumatoid arthritis (RA) is a disease dominated by joint inflammation, accompanied by several peripheral inflammatory manifestations (1). Although the etiology of RA is still not fully understood, the pathogenesis is known to involve chronic synovitis leading to destruction of joint tissues (in particular, cartilage and bone) and consequently, serious impairment of joint function (2). Patients also exhibit features of systemic inflammation (such as marked acute-phase responses), and the disease is associated with autoimmune responses, the latter being most clearly displayed in the production of autoantibodies against the IgG Fc regions (rheumatoid factor)(3).
The important role of T helper cells, macrophages, dendritic cells (DC), and B cells in local tissue destruction in RA has been described extensively (4–7)(summarized in Figure 1). Macrophages and DC in the RA joint contribute strongly to inflammation by the production of proinflammatory mediators, uptake of (auto-) antigen, and presentation of peptides of processed antigen to T helper cells by class II major histocompatibility complex (MHC) molecules (HLA–DR1 and HLA–DR4, which are linked to RA) together with costimulatory molecules. In addition to the cell–cell contact of T helper cells with macrophages and DC, there are a number of factors that cause costimulation of T helper cells (eg,
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