Lin Y, Kirby J A, Browell D A, Morley A R, Shenton B K, Proud G, Taylor R M
Department of Surgery, Medical School, University of Newcastle upon Tyne, UK.
Clin Exp Immunol. 1993 Apr;92(1):145-51. doi: 10.1111/j.1365-2249.1993.tb05961.x.
The interaction between vascular cell adhesion molecule-1 (VCAM-1) and very late antigen-4 (VLA-4) is known to play an important role in stabilizing the adhesion of lymphocytes to endothelial cells. Such cellular adhesion is crucial to many immunological processes including lymphocyte-mediated cell lysis. In this study the expression of VCAM-1 on renal tubular epithelial cells is demonstrated on biopsy sections recovered during acute renal allograft rejection. Experiments performed using epithelial cells cultured from renal tubules show that VCAM-1 is up-regulated by addition of the inflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). Combination of TNF-alpha and IFN-gamma synergized to induce high levels of VCAM-1 expression. Further experiments demonstrated that the cytokines produced by activated lymphocytes in mixed leucocyte culture also up-regulate expression of VCAM-1. Assays of the adhesion of lymphoid cells to cultured renal epithelial cells showed that cytokine pretreatment of the renal cells enhanced the binding of lymphoid cells. The proportion of bound lymphoid cells was significantly reduced by addition of an antibody capable of blocking the interaction of VCAM-1 with VLA-4. This result indicated that the VCAM-1 induced on renal epithelial cells by inflammatory cytokines is functionally capable of binding VLA-4, thereby enhancing the adhesion of potentially graft-damaging lymphoid cells.
血管细胞黏附分子-1(VCAM-1)与极迟抗原-4(VLA-4)之间的相互作用在稳定淋巴细胞与内皮细胞的黏附中起着重要作用。这种细胞黏附对包括淋巴细胞介导的细胞裂解在内的许多免疫过程至关重要。在本研究中,在急性肾移植排斥反应期间回收的活检切片上证实了肾小管上皮细胞上VCAM-1的表达。使用从肾小管培养的上皮细胞进行的实验表明,添加炎性细胞因子肿瘤坏死因子-α(TNF-α)和干扰素-γ(IFN-γ)可上调VCAM-1的表达。TNF-α和IFN-γ的组合协同诱导高水平的VCAM-1表达。进一步的实验表明,混合白细胞培养中活化淋巴细胞产生的细胞因子也上调VCAM-1的表达。对淋巴细胞与培养的肾上皮细胞黏附的测定表明,对肾细胞进行细胞因子预处理可增强淋巴细胞的结合。添加能够阻断VCAM-1与VLA-4相互作用的抗体可显著降低结合的淋巴细胞比例。该结果表明,炎性细胞因子在肾上皮细胞上诱导的VCAM-1在功能上能够结合VLA-4,从而增强潜在的移植损伤性淋巴细胞的黏附。