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We follow with interest, evidence published in this Journal concerning the sensitivities to apoptosis of effector and regulatory T cells (Treg) in inflammatory bowel disease (IBD), as a possible mechanism of breakdown in self-tolerance.1–4 The persistent and relapsing pattern of IBD might originate from outstanding resistance of human enteric cells to apoptosis5 or excessive apoptosis of Treg.3 Thus, therapeutic approaches aiming to restore enteric immune homeostasis should either delete effector cells or improve Treg survival, though it is unclear whether Treg apoptosis is causative or a consequence of enteric autoimmunity in IBD patients.3 Targeted deletion of effector cells has been achieved with a fusion protein composed of interleukin-2 (IL-2, internalisation moiety) and active caspase-2 (apoptotic molecule), bypassing the apparent defective caspase function in colitogenic cells.6 We reasoned that Treg endowed with enhanced killing activity might significantly attenuate the course of inflammatory colitis by shifting the effector/suppressor balance.
In prior studies, we showed that administration of relatively small numbers of Treg decorated with Fas-ligand (FasL) protein (killer Treg), but not naïve Treg, delays the onset of hyperglycaemia in prediabetic non-obese diabetic …
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