ABSTRACT
I. INTRODUCTION Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disease that causes substantial morbidity and accelerated mortality in affected patients ( l ,2). Beginning with the identification of rheumatoid factor in the middle of this century, it has become increasingly evident that the hallmark pathophysiological abnormality in RA is impaired regulation of the immune system. Although alterations in various cell types and soluble mediators have been identified in patients with RA, it appears that T cells are particularly important in this "autoimmune disease." Data from a myriad of studies suggest that CD4+ T lymphocytes subserve a pivotal role in the initiation and perpetuation of the immunologically driven inflammation characteristic of RA (1,3,4). Therefore, a conceptually attractive approach to the treatment of RA targets T cells. There are sundry techniques by which the number or function ofT cells may be modulated. This includes medications and biological agents that limit T-cell cytokine function and monoclonal antibodies (MAb) that diminish T-cell number or function (5,6). Experiences with several such agents are reviewed in other chapters.
