Abstract
Class II major histocompatibility complex (MHC) transplantation antigens constitute, in addition to a processed antigen and the T cell receptor, the trimolecular 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 — taken together — convincing findings. Genetic data suggest that the linkage between RA and human leukocyte antigen (HLA) genes can be traced back to structural differences in distinct MHC class I subunits [2]. A massive increase in class II expressing cells as well as in activated T cells in the inflamed synovial tissue indicate that local class II-dependent T cell activation can take place in synovial tissue [3–5]. Treatment with human immunoglobulin fractions enriched for anti-class II antibodies [6] as well as with mouse anti-CD 4 monoclonal antibodies [7] may diminish disease activity in RA.
Experimental studies from our laboratory that are discussed in this article were supported by grants from the Swedish Medical Research Council, from King Gustaf V:s 80-years foundation, from the Swedish Association against Rheumatism and from the Swedish Agency for Technical Development.
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Klareskog, L. (1992). Role and Regulation of Synovial MHC Class II Antigens in Rheumatoid Arthritis and Related Diseases. 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_8
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DOI: https://doi.org/10.1007/978-3-642-76189-8_8
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