T cell islet accumulation in type 1 diabetes is a tightly regulated, cell-autonomous event.
T cell islet accumulation in type 1 diabetes is a tightly regulated, cell-autonomous event.
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DOI：
10.1016/j.immuni.2009.07.008
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发表时间：
2009-10-16
期刊：
影响因子：
32.4
通讯作者：
Vignali, Dario A. A.
中科院分区：
文献类型：
--
作者：
Lennon, Greig P.;Bettini, Maria;Burton, Amanda R.;Vincent, Erica;Arnold, Paula Y.;Santamaria, Pere;Vignali, Dario A. A.
I型糖尿病是一种T细胞介导的自身免疫性疾病，其特征在于胰岛的淋巴细胞浸润。目前认为胰岛抗原特异性不是进入胰岛的必要条件，并且致糖尿病T细胞可以募集异质性旁观者T细胞群。我们通过产生表达两种不同T细胞群的TCR逆转录小鼠直接测试了这一假设。通过结合致糖尿病和非致糖尿病和/或非自身抗原特异性T细胞，我们证明旁观者T细胞不能在胰岛中积累。自身抗原特异性T细胞在胰岛中积累，但不引起糖尿病，也不受致糖尿病T细胞的存在的影响。此外，67%的从NOD胰岛浸润性CD 4 + T细胞克隆的TCR在逆转录小鼠中表达时能够介导细胞自主性胰岛浸润和/或糖尿病。因此，胰岛进入/积累似乎是细胞自主和严格调节的事件，并受胰岛抗原特异性的控制。
Type I diabetes is a T cell-mediated autoimmune disease, characterized by lymphocytic infiltration of the pancreatic islets. It is currently thought that islet antigen-specificity is not a requirement for islet entry and that diabetogenic T cells can recruit a heterogeneous bystander T cell population. We tested this assumption directly by generating TCR retrogenic mice expressing two different T cell populations. By combining diabetogenic and non-diabetogenic and/or non-autoantigen specific T cells, we demonstrate that bystander T cells cannot accumulate in the pancreatic islets. Autoantigen specific T cells which accumulate in islets, but do not cause diabetes, were also unaffected by the presence of diabetogenic T cells. Additionally, 67% of TCRs cloned from NOD islet-infiltrating CD4+ T cells were able to mediate cell-autonomous islet infiltration and/or diabetes when expressed in retrogenic mice. Therefore islet entry/accumulation appears to be a cell-autonomous and tightly-regulated event and is governed by islet antigen specificity.
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影响因子：
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发表时间：
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