Type 1 diabetes(T1D)results from autoimmune destruction of insulin-producing b-cells in the pancreatic islets.There is an immediate need to restore both b-cell function and immune tolerance to control disease progress...Type 1 diabetes(T1D)results from autoimmune destruction of insulin-producing b-cells in the pancreatic islets.There is an immediate need to restore both b-cell function and immune tolerance to control disease progression and ultimately cure T1D.Currently,there is no effective treatment strategy to restore glucose regulation in patients with T1D.FoxP3-expressing CD4^(+) regulatory T cells(Tregs)are potential candidates to control autoimmunity because they play a central role in maintaining self-tolerance.However,deficiencies in either naturally occurring Tregs(nTregs)themselves and/or their ability to control pathogenic effector T cells have been associated with T1D.Here,we hypothesize that nTregs can be replaced by FoxP3^(+) adaptive Tregs(aTregs),which are uniquely equipped to combat autoreactivity in T1D.Unlike nTregs,aTregs are stable and provide long-lived protection.In this review,we summarize the current understanding of aTregs and their potential for use as an immunological intervention to treat T1D.展开更多
基金supported by grants from the National Institutes of Health (NIH,AI081238)Juvenile Diabetes Research Foundation (JDRF,31-2008-353).
文摘Type 1 diabetes(T1D)results from autoimmune destruction of insulin-producing b-cells in the pancreatic islets.There is an immediate need to restore both b-cell function and immune tolerance to control disease progression and ultimately cure T1D.Currently,there is no effective treatment strategy to restore glucose regulation in patients with T1D.FoxP3-expressing CD4^(+) regulatory T cells(Tregs)are potential candidates to control autoimmunity because they play a central role in maintaining self-tolerance.However,deficiencies in either naturally occurring Tregs(nTregs)themselves and/or their ability to control pathogenic effector T cells have been associated with T1D.Here,we hypothesize that nTregs can be replaced by FoxP3^(+) adaptive Tregs(aTregs),which are uniquely equipped to combat autoreactivity in T1D.Unlike nTregs,aTregs are stable and provide long-lived protection.In this review,we summarize the current understanding of aTregs and their potential for use as an immunological intervention to treat T1D.
