Immunopathology of Rheumatoid Synovium
The character of the immunologically stimulated chronic inflammatory infiltrate is to a considerable extent determined by nonspecific factors governing mononuclear cell traffic. The volume, composition, and distribution of this traffic is strongly dependent on an initial adhesive interaction between circulating mononuclear cells and the EC of the postcapillary venules (PCV) of the involved tissues. The emigration of lymphocytes from the PCV is preceded by binding of the lymphocytes to the endothelial lining cell. This binding is enhanced by lymphokines (IFN-γ, TNF-β, IL-4) and monokines (IL-1, TNF-α), secreted by perivascular inflammatory cells and acting on the EC. This enhancement may permit an initial, immunologically generated small focus of mononuclear cells to amplify itself to a larger infiltrate. Two general mechanisms appear to be operative in chronic inflammation: (1) a specific mechanism in which an antigen stimulates an immune response with an initial secretion of cytokines, and (2) a nonspecific mechanism in which the cytokines released mediate a largely nonspecific infiltration of chronic inflammatory cells. The specific mechanism may determine the site of the inflammatory response and the nature of the antibodies which may be locally synthesized. The nonspecific mechanism creates the conventional pattern of chronic inflammation observed in variable sites in a number of diseases.
KeywordsSynovial Fluid Atopic Dermatitis High Endothelial Venule Rheumatoid Synovium Human Dermal Microvascular Endothelial Cell
Unable to display preview. Download preview PDF.
- 29.Douby AD, Sinclair AK, Osborne-Lawrenc SL, Zeldes W, Kan L, Fox DA (1989) Clonal heterogeneity of synovial fluid T lymphocytes from patients with rheumatoid arthritis (abstract). Arthritis Rheum 32:B44Google Scholar
- 30.Dier DL, Roessner KD, Cooper SM (1989) Diversity of rheumatoid tissue T cells by T cell receptor analysis (abstract). Arthritis Rheum 32:B43Google Scholar
- 32.Smith SH, Brown MH, Rowe D, Callard RE, Beverley PCL (1986) Functional subsets of human helper-inducer cells defined by a new monoclonal antibody, UCHL-1. Immunology 58:53–70Google Scholar
- 37.Duke O, Panayi GS, Bofill M, Poulter L, Janossy G (1986) Evidence for a deficiency of the suppressor-inducer T cell subset in the synovial membrane in rheumatoid arthritis (abstract). Br J Rheumatol 25 (Suppl 65):38Google Scholar
- 40.Ishikawa N, Eguchi K, Otsubo T, Ueki Y, Fukuda T, Tezuka H, Matsunaga M, Kawabe Y, Shimomura C, Izumi M, Ban Y, Ito K, Nagataki S (1987) Reduction in the suppressor-inducer T cell subset and increase in the helper T cell subset in thyroid tissue from patients with Graves’ disease. J Clin Endocrinol Metab 65:17–23PubMedCrossRefGoogle Scholar
- 42.Ford DK, Da Roza D (1987) Further observations on the response of synovial lymphocytes to viral antigens in rheumatoid arthritis. J Rheumatol 13:113–117Google Scholar
- 43.Ford DK, Da Roza D, Shah P (1980) Cellmediated immune responses of synovial mononuclear cells to sexually transmitted enteric and mumps antigens with Reiter’s syndrome, rheumatoid arthritis and ankylosing spondylitis. J Rheumatol 8:220–232Google Scholar
- 44.Ford DK, DaRoza DM, Reid GD, Chantler JK, Tingle AJ (1981) Synovial mononuclear cell responses to rubella antigen in rheumatoid arthritis and unexplained persistent knee synovitis. J Rheumatol 9:420–423Google Scholar
- 46.Gaston JSH, Life PF, Granfors K, Merilahti-Palo R, Bailey L, Consalvey S, Toivanen A, Bacon PA (to be published) Synovial T lymphocyte recognition of organisms which trigger reactive arthritisGoogle Scholar
- 47.Padula SJ, Pfister RD (1988) Lyme disease synovial fluid cells show significantly greater response to Borrelia Burgdorferi antigens than peripheral cells (abstract). Clin Res 36:535 AGoogle Scholar