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A series of excellent articles published recently in Gut have evaluated the role of T regulatory (Treg) cells in inflammatory bowel disease (IBD) and surrogate animal models.1 2 In principle, self-tolerance in autoimmune disorders may be restored either by specific interference with effector cells and molecular pathways involved in immune activation, or selective enhancement of suppressive cells and cytokines. Based on the long-standing recognition that interleukin 2 (IL2) is a significant stimulatory cytokine involved in immune activation, interference with IL2 signalling has been considered as a potential approach to arrest autoimmunity. Stimulated lymphocytes (B and cytotoxic T cells) secrete IL2 and express the IL2 receptor α chain (CD25) within a positive feedback loop of activation. More physiological approaches to reinstitution of self-tolerance surround the activity of suppressive immune cells, in particular, Treg cells, which prevent and even reverse ongoing autoimmune reactions.3 4 5 6 One particular potent subset of naturally occurring Treg cells is characterised by CD25 expression at high levels in conjunction with transcription factor X-linked forkhead/winged helix (FoxP3). It is not only a contextual relationship between CD25 and suppressive mechanisms, but ample supply of IL2 is essential to the development and function of these Treg cells, and inhibition of IL2 production by cytotoxic cells is one of the primary mechanisms of suppression. Therefore, disruption of IL2 signalling that tilts the equilibrium against suppressive elements evolves as a deleterious mechanism in the context of autoimmunity, rather than an immunosuppressive strategy. Consistently, mice deficient in IL2 …
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