Titlebook: Rheumatoid Arthritis; Recent Research Adva Josef S. Smolen,Joachim R. Kalden,Ravinder N. Main Conference proceedings 1992 Springer-Verlag B

BLA

Is Rheumatoid Arthritis a Disappearing Disease?rs. Compared to osteoarthritis, however, paleopathological evidence from skeletal remains of its early existence is difficult to obtain. It was hypothesized over 10 years ago [1] that RA, commonly agreed to be triggered by a virus, could behave like other major chronic infectious diseases, many of w

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Genetic Factors in Rheumatoid Arthritisuding an oligo- or polygenic component. Given the massive investment of resources in this field of rheumatology research it is saluatory to consider data which suggest the genetic component may account for as little as 12% of the total variability [1]. Genetic studies, however, should not be dismiss

CLAN

歪曲道理

Pathogenesis of Rheumatoid Arthritis: Cellular and Cytokine Interactionsarticular and systemic complications. The basic aetiology of this disease is not known, but there is a clear genetic predisposition. This maps clearly, but not exclusively, to the HLA-DR region; however, genetic predisposition is not sufficient to explain the disease, as identical twins are often (~

Abominate

Role of Cellular Adhesion in Rheumatoid Synovitisf this reaction, cytokines and growth factors are released which mediate a nonspecific amplification of the initial inflammatory focus, proliferation of the synovial tissue, and immunoglobulin and rheumatoid factor synthesis.

Oafishness

Endothelial Cells and Dendritic Cells in Rheumatoid Inflammation the synovial tissue by first binding to the high endothelial venules. Certain cytokines increase this binding and direct the cell traffic to the inflammatory sites. Interferon-γ stimulates EC to express HLA class-II molecules and to become accessory cells for T-cell activation. The dendritic cells

coagulation

GLIDE

Role and Regulation of Synovial MHC Class II Antigens in Rheumatoid Arthritis and Related Diseasesrimolecular complex which governs most T cell-dependent immune reactions [1]. Evidence that MHC class II-dependent T lymphocyte activation is critically involved in the pathogenesis of rheumatoid arthritis (RA) as well as in other inflammatory arthritides derives from a series of indirect but — take

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CD5+ B Cells and Double-Negative T Cells in Rheumatoid Arthritise immune system may be important in the development of the disease [70]. This in turn led to intensive studies on the cells involved and their interactions and homing to the site of local inflammation. In RA, the synovial membrane is characterized by the presence of lymphoid aggregates, local produc

Libido

The Genetics of Rheumatoid Factors (RF): The V-gene Repertoire of RFs in Rheumatoid Arthritis as Ananship between rheumatoid factors and clinical symptoms of rheumatoid arthritis (RA) occurred 50 years ago [53]. The pioneering phase between 1940 and 1950 included the confirmation of Waaler’s findings by Rose and collaborators [see 50]. This period brought an appreciation of the diagnostic signific