B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes
B7/CD28 costimulation is essential for the homeostasis of the CD4+CD25+ immunoregulatory T cells that control autoimmune diabetes
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DOI：
10.1016/s1074-7613(00)80195-8
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发表时间：
2000-04-01
期刊：
影响因子：
32.4
通讯作者：
Bluestone, JA
中科院分区：
文献类型：
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作者：
Salomon, B;Lenschow, DJ;Bluestone, JA
CD28/B7共刺激与自身免疫性疾病的诱发和进展有关。在实验诱导的自身免疫模型中，已表明在CD28共刺激缺陷的小鼠中，自身免疫的发生可被预防或强度降低。与之形成鲜明对比的是，在B7 - 1/B7 - 2缺陷和CD28缺陷的NOD小鼠中，自发性糖尿病会加重。这些小鼠的免疫调节性CD4(+)CD25(+) T细胞显著减少，而这种细胞在糖尿病前期的NOD小鼠中可控制糖尿病。CD28基因敲除（CD28KO）和B7 - 1/B7 - 2基因敲除（B7 - 1/B7 - 2KO）小鼠都缺乏这种细胞，将这种调节性T细胞亚群从对照NOD动物转移到CD28缺陷动物体内可延缓/预防糖尿病。结果表明，CD28/B7共刺激通路对于控制自发性自身免疫疾病的调节性T细胞的发育和内稳态至关重要。
CD28/B7 costimulation has been implicated in the induction and progression of autoimmune diseases. Experimentally induced models of autoimmunity have been shown to be prevented or reduced in intensity in mice rendered deficient for CD28 costimulation. In sharp contrast, spontaneous diabetes is exacerbated in both B7-1/B7-2-deficient and CD28-deficient NOD mice. These mice present a profound decrease of the immunoregulatory CD4(+)CD25(+) T cells, which control diabetes in prediabetic NOD mice. These cells are absent from both CD28KO and B7-1/B7-2KO mice, and the transfer of this regulatory T cell subset from control NOD animals into CD28-deficient animals can delay/prevent diabetes. The results suggest that the CD28/B7 costimulatory pathway is essential for the development and homeostasis of regulatory T cells that control spontaneous autoimmune diseases.