IL2 and Autoimmunity: IL-2 and the transcription factor STAT5, downstream of IL-2 receptor (IL-2R), induce the expression of Foxp3 and differentiation of tTregs.60 Furthermore, STAT5 activation driven by IL-2R signalling enhances the suppressor function of differentiated Tregs.61 An absence of IL-2 signalling has been shown to reduce the number and functional activity of Tregs, predisposing to autoimmunity and inflammation.62 63 The structural conformation of IL-2R in Tregs provides a competitive advantage for IL-2-receptor engagement over alternative cell subsets.