Miller Michelle M, Fogle Jonathan E, Ross Peter, Tompkins Mary B
Immunology Program, North Carolina State University, Raleigh, NC 27607, USA.
AIDS Res Hum Retroviruses. 2013 Apr;29(4):641-51. doi: 10.1089/aid.2012.0322. Epub 2013 Feb 1.
Using the feline immunodeficiency virus (FIV) model for AIDS-lentivirus infection, our laboratory has previously demonstrated that T regulatory (Treg) cell-mediated immune T and B cell dysfunction contributes to lentivirus persistence and chronic disease through membrane bound transforming growth factor beta (mTGFb). Studying Treg cells in the context of infection has been problematic as no inducible marker for activated Treg cells had been identified. However, recent reports in human Treg studies have described a novel protein, glycoprotein A repetitions predominant (GARP), as a unique marker of activated human Treg cells that anchors mTGFb. Herein we extend these studies to the feline Treg system, identifying feline GARP and demonstrating that human and feline GARP proteins are homologous in structure, expression pattern, and ability to form a complex with TGFb. We further demonstrate that GARP and TGFb form a complex on the surface of activated Treg cells and that these GARP(+)TGFb(+) Treg cells are highly efficient suppressor cells. Analysis of expression of this Treg activation marker in the FIV-AIDS model reveals an up-regulation of GARP expressing Treg cells during chronic FIV infection. We demonstrate that the GARP(+) Treg cells from FIV-infected cats suppress T helper cells in vivo and that blocking GARP or TGFb eliminates this suppression. These data suggest that GARP is expressed in complex with TGFb on the surface of activated Treg cells and plays an important role in TGFb(+) Treg-mediated T cell immune suppression during lentivirus infection.
利用猫免疫缺陷病毒(FIV)模型研究艾滋病慢病毒感染,我们实验室先前已证明,调节性T(Treg)细胞介导的免疫T和B细胞功能障碍通过膜结合转化生长因子β(mTGFβ)导致慢病毒持续存在和慢性疾病。由于尚未鉴定出活化Treg细胞的诱导性标志物,因此在感染背景下研究Treg细胞一直存在问题。然而,最近关于人类Treg研究的报告描述了一种新蛋白,即主要的糖蛋白A重复序列(GARP),作为活化人类Treg细胞的独特标志物,它能锚定mTGFβ。在此,我们将这些研究扩展到猫Treg系统,鉴定出猫GARP,并证明人类和猫GARP蛋白在结构、表达模式以及与TGFβ形成复合物的能力方面是同源的。我们进一步证明,GARP和TGFβ在活化Treg细胞表面形成复合物,并且这些GARP(+)TGFβ(+) Treg细胞是高效的抑制细胞。在FIV艾滋病模型中对这种Treg活化标志物表达的分析揭示,在慢性FIV感染期间,表达GARP的Treg细胞上调。我们证明,来自FIV感染猫的GARP(+) Treg细胞在体内抑制辅助性T细胞,并且阻断GARP或TGFβ可消除这种抑制作用。这些数据表明,GARP在活化Treg细胞表面与TGFβ形成复合物表达,并在慢病毒感染期间TGFβ(+) Treg介导的T细胞免疫抑制中发挥重要作用。