Institute of Medical Mircobiology, University Hospital Essen, Essen, Germany.
Genes Immun. 2010 Jun;11(4):357-61. doi: 10.1038/gene.2010.5. Epub 2010 Mar 4.
Most recently, we have described the G-protein coupled receptor 83 (GPR83), which is highly expressed by CD4(+)CD25(+) regulatory T cells (Tregs) to be involved in the induction of CD4(+)Foxp3(+) Tregs in the course of an ongoing immune response. Four GPR83 isoforms have been described. Here, we have shown that GPR83 isoform-4, which differs from GPR83 isoform-1 by 20 additional aminoacids in the second cytoplasmatic loop, is predominantly expressed by Tregs. Interestingly, GPR83 isoform-4 but not GPR83 isoform-1 retrovirally transduced T cells were able to interfere with inflammatory responses in vivo. Re-analysis of GPR83 transduced T cells revealed that this in vivo acquisition of suppressive activity was associated with the induction of Treg-associated molecules including Foxp3 in GPR83 isoform-4 but not GPR83 isoform-1 transduced CD4(+) T cells under inflammatory conditions. Our results suggest that the 20 additional aminoacids within GPR83 isoform-4 are involved in Treg induction during inflammatory immune responses.
最近，我们描述了 G 蛋白偶联受体 83（GPR83），它在正在进行的免疫反应过程中高度表达于 CD4+CD25+调节性 T 细胞（Tregs），参与 CD4+Foxp3+Tregs 的诱导。已经描述了四种 GPR83 同工型。在这里，我们表明，与 GPR83 同工型-1 相比，第二胞质环中多出 20 个氨基酸的 GPR83 同工型-4 主要由 Tregs 表达。有趣的是，GPR83 同工型-4 而不是 GPR83 同工型-1 逆转录病毒转导的 T 细胞能够在体内干扰炎症反应。对 GPR83 转导的 T 细胞的重新分析表明，这种体内获得的抑制活性与 Treg 相关分子的诱导有关，包括 Foxp3 在 GPR83 同工型-4 中，但在炎症条件下 GPR83 同工型-1 转导的 CD4+T 细胞中则没有。我们的结果表明，GPR83 同工型-4 中的 20 个额外氨基酸参与了炎症免疫反应中 Treg 的诱导。
