Abstract

Rheumatoid arthritis is an oft debilitating chronic disease of an autoimmune nature. Although the putative antigen remains unknown, the recent elucidation of the structure and functional relationships of the trimolecular complex governing the immune response to antigen, facilitates the development of novel approaches to the treatment of RA and enhances our understanding of the etiopathogenesis of this disorder and autoimmunity in general. The characterization of immune active T cell populations, particularly at inflammatory sites such as the synovium, with respect to their expressed and genomic TCR repetoire, may permit the identification of crucial genetic components which contribute either directly or indirectly to the susceptibility and/or the development of RA.

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