Vaessen L M, Schipper F, Knoop C, Claas F H, Weimar W
Department of Internal Medicine I, University Hospital Rotterdam-Dijkzigt, The Netherlands.
Clin Exp Immunol. 1996 Jan;103(1):119-24. doi: 10.1046/j.1365-2249.1996.909604.x.
We investigated the levels of TCR-gamma delta T cells and their subpopulations V delta 1 and V delta 2 in the peripheral blood lymphocytes (PBL) of 28 heart transplant (HTx) patients. Patients (n = 10) receiving cyclosporin A (CsA) for treatment of a nephrotic syndrome (NS) and 10 healthy individuals served as controls. There was no difference in levels of TCR-gamma delta T cells between the different groups. However, an elevated proportion of V delta 1+ gamma delta T cells was found in the PBL of HTx patients, especially when these cells were present in their graft-infiltrating lymphocyte (GIL) cultures. V delta 1+ gamma delta T cells of HTx patients showed normal expression of CD45RO and lacked the activation markers CD25 and HLA-DR. After expanding in IL-2-containing medium, PBL cultures of HTx patients more often were dominated by V delta 1 cells than PBL cultures of controls, in which V delta 2 cells were predominantly grown. The aberrant composition of the TCR-gamma delta population in HTx patients was not a result of immunosuppressive medication, since the proportion V delta 1+ gamma delta T cells was normal in the PBL of the NS patients receiving a similar dose of CsA. It is postulated that long-term antigenic stimulation by the graft, at low level, might be responsible for the altered composition of the gamma delta pool in the HTx patients. Since no donor HLA-specific gamma delta T cells have been detected, other ligands, such as heat shock proteins, may be involved.
我们研究了28例心脏移植(HTx)患者外周血淋巴细胞(PBL)中TCR-γδ T细胞及其亚群Vδ1和Vδ2的水平。10例接受环孢素A(CsA)治疗肾病综合征(NS)的患者及10名健康个体作为对照。不同组之间TCR-γδ T细胞水平无差异。然而,在HTx患者的PBL中发现Vδ1 + γδ T细胞比例升高,尤其是当这些细胞存在于其移植物浸润淋巴细胞(GIL)培养物中时。HTx患者的Vδ1 + γδ T细胞显示CD45RO正常表达,且缺乏活化标志物CD25和HLA-DR。在含白细胞介素-2的培养基中扩增后,HTx患者的PBL培养物比对照组的PBL培养物更常以Vδ1细胞为主,对照组的PBL培养物中主要生长的是Vδ2细胞。HTx患者TCR-γδ群体的异常组成并非免疫抑制药物所致,因为接受相似剂量CsA的NS患者的PBL中Vδ1 + γδ T细胞比例正常。据推测,移植物长期低水平的抗原刺激可能是HTx患者γδ库组成改变的原因。由于未检测到供体HLA特异性γδ T细胞,可能涉及其他配体,如热休克蛋白。