The polyubiquitin-binding domain of ABIN1 limits TLR-induced MyD88 signaling to prevent spontaneous autoimmunity in mice.

Objective. CD4؉,CD25high regulatory T (Treg) cells play a crucial role in the maintenance of self tolerance and prevention of organ-specific autoimmunity. high ,CD127 ؊/low nTreg cells. Furthermore, a significant inverse correlation was observed between the extent of T cell regulation in suppressor assays and the level of lupus disease activity.Conclusion. This study is the first to show that, in human SLE, impaired sensitivity of Tresp cells to the suppressive effects of a comparably functional, highly purified nTreg cell population leads to a defective suppression of T cell proliferation in active SLE. Studies aiming to define the mechanisms leading to Tresp cell resistance might help in the development of highly specific, alternative immunotherapeutic tools for the control of systemic autoimmune diseases such as SLE.Immune homeostasis is controlled by mechanisms of central and peripheral tolerance. Central tolerance involves the deletion of self-reactive T cells in the thymus at an early stage of development (1,2). Peripheral tolerance is maintained by, among other mechanisms, a unique subset of naturally occurring CD4ϩ, CD25ϩ natural regulatory T (nTreg) cells in the mouse, which are able to suppress activation and effector functions of autoreactive T cells that have escaped other mechanisms of tolerance (3-5).

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