Antiperinuclear factor, a marker autoantibody for rheumatoid arthritis: colocalisation of the perinuclear factor and profilaggrin

Article Abstract:

Most of the rheumatic diseases have an autoimmune basis, in which the body inappropriately makes antibodies against its own tissues. Some of these autoantibodies are specifically associated with a disease and are useful in diagnosis, as is the case with systemic lupus erythematosus and polymyositis. Although rheumatoid factors, antibodies directed against a portion of the stem structure found on all antibodies, are present in many patients with rheumatoid arthritis, they are also found in patients with other autoimmune diseases and even in healthy people. Three other autoantibodies associated with rheumatoid arthritis have been described. One of them is antiperinuclear factor, in which antibodies are directed against a molecule found in human buccal (cheek muscle) mucosal cells. The test for antiperinuclear factor was modified, resulting in detection of the factor in more rheumatoid patients but not in more healthy subjects. The modified test also gave more reproducible results. The test was positive in 51 of 63 rheumatoid patients, but was also positive in 21 to 29 percent of patients with systemic lupus erythematosus, systemic scleroderma, and Sjogren's syndrome. The factor which antiperinuclear factor binds to could not be identified, but binding was localized to granules in the mucosal cells that contain a dense mixture of proteins. Profilaggrin, a protein found in specialized cells, shares the same localization in the buccal cells as perinuclear factor, but the two factors are not identical. The study provides a basis for study of the significance of antiperinuclear factor in rheumatoid arthritis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Usage, Immunofluorescence, Fluorescent antibody technique

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Effects of interferon gamma on cultured synovial cells from patients with rheumatoid arthritis: inhibition of cell growth, prostaglandin E2, and collagenase release

Article Abstract:

Interferons are proteins produced when cells are exposed to viral or other foreign nucleic acids. Interferon gamma (IFN-gamma) was shown to prevent the proliferation of cells, to alter the immune system, and to prevent the activity of viruses. Studies have also indicated that artificially produced recombinant IFN-gamma (rIFN-gamma) may be effective in treating rheumatoid arthritis (RA), an inflammatory joint disease. RA is characterized by the overgrowth of synovial cells and fibroblasts, as well as the accumulation of various types of defense cells including lymphocytes, monocytes, and macrophages. In addition, inflamed tissues within the RA joint release interleukin-1 (IL-1), which causes the release of factors involved in tissue degradation, including collagenase and prostaglandins, such as prostaglandin E2 (PGE2). The effects of rIFN-gamma on the growth of fibroblast-like cells in the synovial lining of patients with RA were assessed. The effects of rIFN-gamma on the release of collagenase and prostaglandins from cells activated by recombinant IL-1-beta (rIL-1-beta) were also examined. Recombinant IFN-gamma prevented the growth of synovial cells from six of nine samples and the release of collagenase and prostaglandins from synovial cells activated by recombinant IL-1-beta. There was no relation between the effects of rIFN-gamma on cell overgrowth and prostaglandin synthesis or PGE2 release. (Consumer Summary produced by Reliance Medical Information, Inc.)

Interferon gamma, Synovial membranes, Synovial membrane

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