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The main function(s) of Treg cells is to suppress activation of other T-cell members that are specific for those self-antigens [1,2]. Thus, negative selection is the main mechanism which produces central tolerance and as such negative selection affects self-reactive CD4+ and CD8+ cells that recognize self-peptides in the context of class II MHC and class I MHC, respectively. In contrast, activation of peripheral tolerance as distinct from central tolerance occurs when T-cells that have reached maturity recognize self-antigens. This event results in T-cell inactivation (aka anergy) or even cell death when these T-cells are acted on by Treg cells. In that regard, it is obvious that in order to prevent T-cell responses to selfantigens that are not thymus-related, the activity of Treg cells becomes crucial for allaying autoimmune responses especially when central tolerance is compromised. Furthermore, it can now be shown that loss of Treg function(s) is a significant contributor to autoimmunity as was shown to be the case in rheumatoid arthritis (RA) [3-7] as well as in other autoimmune disorders, such as inflammatory bowel disease (IBD) [8] and psoriasis [9]. For example, in inflammatory arthritis, IBD, multiple sclerosis, Type 1 diabetes, etc. effector T-helper cells classified as regulatory T cells consists of 2 types, mainly FoxP3+-expressingand Type 1 Regulatory (TR1) cells. TR1 cells are identified by 2 molecular markers, namely, lymphocyte activation gene 3 and CD49b, and also express interleukin-10 [10]. Both regulatory cell types behave as termination of immune response cells [8]. Importantly, the TR1-type regulatory T-cells are decreased and their function impaired in autoimmune diseases.

Recent Advances Show That Abnormal T-Regulatory Cell Function Perpetuates Chronic Inflammatory Arthritis