الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Rheumatoid arthritis is a chronic, inflammatory, autoimmune disease that mostly affects the joints and is characterized by autoantibodies that target numerous molecules. It is a disease with a wide range of clinical manifestations and pathogenetic pathways. Recently, early diagnosis, intensive treatment, and expanded therapeutic choices of DMARDS have significantly improved both the management and long-term prognosis of RA.
T cells play a key role in the pathophysiology of RA, which is therefore considered a typical T‑cell‑mediated disease. Regulatory T cells (Tregs) are another kind of T cells that have suppressive capabilities and are thought to protect against the autoimmune response. Both qualitative and quantitative deficiencies of Tregs have been implicated in the development of the autoimmune pathology in many diseases.
Sakaguchi et al, were the first to spark interest in Treg cells by identifying a population of CD4+T cells that strongly express CD25 and prevent autoimmunity in a murine model.
The identification of FoxP3 as a major regulator for Tregs provided a significant marker for this T-cell fraction. Although the notion of Tregs playing a protective function in autoimmunity is largely acknowledged, data regarding RA and SLE are inconsistent.
The first-line pharmacotherapy for RA is low-dose MTX. It exerts anti-inflammatory effects via maintaining high extracellular adenosine levels (ADO).
Tregs suppress a wide range of immune cells activation, proliferation, and effector functions through multiple mechanisms. One of these methods is through extracellular ADO synthesis mediated by CD39/CD73, which are abundantly expressed on the surface of Tregs. FoxP3+ regulatory T cells that express high levels of CD39 and CD73, are capable of generating extracellular adenosine from ATP, and may be the only T cells that have the full enzymatic machinery necessary to do so.