Delneste Y, Jeannin P, Gosset P, Lassalle P, Cardot E, Tillie-Leblond I, Joseph M, Pestel J, Tonnel A B
Unité INSERM U 416, Institut Pasteur, Lille, France.
Clin Exp Immunol. 1995 Jul;101(1):164-71. doi: 10.1111/j.1365-2249.1995.tb02293.x.
Adhesion of inflammatory cells to endothelium is a critical step for their transvascular migration to inflammatory sites. To evaluate the relationship between T lymphocytes (TL) and vascular endothelium, supernatants from allergen-stimulated TL obtained from patients sensitive to Dermatophagoides pteronyssinus (Dpt) versus healthy subjects were added to endothelial cell (EC) cultures. TL were stimulated by autologous-activated antigen-presenting cells (APC) previously fixed in paraformaldehyde to prevent monokine secretion. Two parameters were measured: the expression of adhesion molecule and the production of IL-6. Related allergen-stimulated TL supernatants from allergic patients induced an increase of VCAM-1 and intercellular adhesion molecule-1 (ICAM-1) expression when supernatants of the control groups (TL exposed to an unrelated allergen or not stimulated or TL obtained from healthy subjects) did not. E-selectin expression was not modulated whatever the supernatant added to EC culture. IL-6 production by EC was significantly enhanced after activation with related allergen-stimulated TL supernatants from allergics compared with control supernatants. Induction of VCAM-1 expression was inhibited by adding neutralizing antibodies against IL-4, whereas IL-6 production and ICAM-1 expression were inhibited by anti-interferon-gamma (IFN-gamma) antibodies. Enhanced production of IL-4 and IFN-gamma was detected in related allergen-stimulated TL supernatants from allergic subjects compared with the different supernatants. These data suggest that allergen-specific TL present in the peripheral blood of allergic patients are of Th1 and Th2 subtypes. Their stimulation in allergic patients may lead to the activation of endothelial cells and thereby participate in leucocyte recruitment towards the inflammatory site.
炎症细胞与内皮细胞的黏附是其跨血管迁移至炎症部位的关键步骤。为评估T淋巴细胞(TL)与血管内皮之间的关系,将来自对尘螨(Dpt)敏感患者与健康受试者的经变应原刺激的TL上清液添加至内皮细胞(EC)培养物中。TL由先前用多聚甲醛固定以防止单核因子分泌的自体活化抗原呈递细胞(APC)刺激。测量了两个参数:黏附分子的表达和IL-6的产生。当对照组(暴露于无关变应原或未受刺激的TL或来自健康受试者的TL)的上清液未引起变化时,来自过敏患者的相关变应原刺激的TL上清液可诱导血管细胞黏附分子-1(VCAM-1)和细胞间黏附分子-1(ICAM-1)表达增加。无论向EC培养物中添加何种上清液,E-选择素的表达均未受到调节。与对照上清液相比,用来自过敏患者的相关变应原刺激的TL上清液激活后,EC产生的IL-6显著增强。添加抗IL-4中和抗体可抑制VCAM-1表达的诱导,而抗干扰素-γ(IFN-γ)抗体可抑制IL-6的产生和ICAM-1的表达。与不同上清液相比,在来自过敏受试者的相关变应原刺激的TL上清液中检测到IL-4和IFN-γ的产生增加。这些数据表明,过敏患者外周血中存在的变应原特异性TL属于Th1和Th2亚型。它们在过敏患者中的刺激可能导致内皮细胞活化,从而参与白细胞向炎症部位的募集。