Type-II Collagen in the Pathogenesis of Rheumatoid Arthritis

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Rheumatoid Arthritis
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Abstract

Rheumatoid arthritis (RA) is now generally regarded as an autoimmune disease with relapsing or progressive occurrence of arthritis affecting preferentially peripheral joints. In spite of the fact that it is a severe and crippling disease affecting a large population, very little is known of its etiology and pathogenesis, although many of its seconday manifestations have been well described. Fortunately, basic research has made considerable progress which now make it possible (a) to evolve the structural requirements for one critical event of importance in RA, the trimolecular interaction between an autoantigenic peptide on major histocompatibility complex (MHC) class-II molecule and the T-cell receptor, and (b) to rapidly increase our knowledge of the basic rules for self- and non-self-discrimination by the immune system. Analysis of the MHC class-II genes which confer a high risk of develo** RA suggests that many, perhaps a majority of patients suffering from the syndrome classified as RA according to the criteria of the Arthritis Rheumatism Association actually suffer from a single disease entity with a pathologic response to a particular autoantigen. Considering the preferential involvement of peripheral joints in RA, it is likely that this particular antigen is a molecule specifically located in joint tissues. In this chapter the descriptive findings of autoimmune reactions to cartilage-specific type-II collagen (CII) in RA are reviewed and the general requirements for recognition of these molecules by the immune system are discussed.

This work was supported by the Swedish Medical Research Council, the Craaford Foundation, the King Gustav V 80-years Foundation, the Nanna Swartz Foundation, and National League against Rheumatism.

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© 1992 Springer-Verlag Berlin Heidelberg

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Holmdahl, R. (1992). Type-II Collagen in the Pathogenesis of Rheumatoid Arthritis. In: Smolen, J.S., Kalden, J.R., Maini, R.N. (eds) Rheumatoid Arthritis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-76189-8_13

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