Ciprandi G, Buscaglia S, Pesce G, Villaggio B, Bagnasco M, Canonica G W
Allergy and Clinical Immunology Service, University of Genoa, Italy.
J Allergy Clin Immunol. 1993 Mar;91(3):783-92. doi: 10.1016/0091-6749(93)90198-o.
Allergic inflammation can be experimentally reproduced in vivo in humans, by means of the conjunctival provocation test with allergen. The allergen stimulation triggers an early clinical response and an almost simultaneous cellular infiltrate. Among the factors that can contribute to the local cellular recruitment, we postulate a possible early involvement of CD54 in the development of inflammation caused by the allergic reaction.
We used a sensitive immunocytochemical immunoenzymatic alkaline phosphatase-monoclonal antialkaline phosphatase technique to detect the possible expression of CD54 molecule on epithelial cells of conjunctiva in 15 allergic subjects and in 15 healthy individuals in basal conditions and after allergen challenge (Parietaria judaica) during the off-pollen season.
At baseline all studied individuals did not evidence CD54 expression on epithelial cells; 30 minutes after allergen challenge, all the allergic individuals showed a marked expression of CD54 on conjunctival epithelium, whereas none of healthy subjects showed any CD54 expression. First, CD54 expression on conjunctival epithelium after specific provocation test appeared as a specific phenomenon occurring only in sensitized subjects; moreover, it is an immediate event concomitant with the local inflammatory infiltrate. Therefore conjunctival epithelium unexpectedly appeared to be more than a bystander in the allergic reaction; it may be perceived as an active participant interacting with the inflammatory infiltrate.
These findings indicate that CD54 may play a central role in the allergic inflammation and strongly support the concept that maneuvers designed to interact with the adhesion machinery expressed on inflammatory cells and epithelium may be a helpful therapeutic approach.
通过过敏原结膜激发试验，可在人体体内通过实验再现变应性炎症。过敏原刺激引发早期临床反应和几乎同时出现的细胞浸润。在可能导致局部细胞募集的因素中，我们推测CD54可能在变应性反应引起的炎症发展中早期就发挥作用。
我们采用敏感的免疫细胞化学免疫酶碱性磷酸酶-单克隆抗碱性磷酸酶技术，检测15名变应性受试者和15名健康个体在花粉淡季基础状态下以及过敏原激发（犹太蓖麻）后结膜上皮细胞上CD54分子的可能表达情况。
在基线时，所有研究个体的上皮细胞均未显示CD54表达；过敏原激发30分钟后，所有变应性个体的结膜上皮均显示CD54的显著表达，而所有健康受试者均未显示任何CD54表达。首先，特异性激发试验后结膜上皮上的CD54表达是仅在致敏个体中出现的特定现象；此外，它是与局部炎症浸润同时发生的即时事件。因此，结膜上皮在变应性反应中出乎意料地似乎不仅仅是旁观者；它可能被视为与炎症浸润相互作用的积极参与者。
这些发现表明CD54可能在变应性炎症中起核心作用，并有力支持了这样的概念，即旨在与炎症细胞和上皮细胞上表达的黏附机制相互作用的操作可能是一种有益的治疗方法。
