Bonini Stefano, Lambiase Alessandro, Sgrulletta Roberto, Bonini Sergio
Interdisciplinary Center for Biomedical Research (CIR) Laboratory of Ophthalmology, University of Rome Campus Bio-Medico, and G.B. Bietti Eye Foundation, Italy.
Curr Opin Allergy Clin Immunol. 2003 Oct;3(5):381-7. doi: 10.1097/00130832-200310000-00011.
The purpose of this review is to describe the new immunopathologic features of vernal keratoconjunctivitis: the involvement of cytokines, growth factors, cells, mediators and neurotransmitters, as well as the mechanism leading to tissue remodelling.
Vernal keratoconjunctivitis is an allergic eye disease affecting young boys living in a warm climate. It is characterized by conjunctival giant papillae, hyperemia and frequent involvement of the cornea. Approximately 50% of the patients with vernal keratoconjunctivitis do not have a family or medical history of atopic diseases, and do not show IgE sensitization, suggesting that this disease is not solely IgE mediated. Vernal keratoconjunctivitis is a Th2 lymphocyte driven disease with a Th2 cytokine derived pattern, increased levels of mRNA for IL-3, IL-4, IL-5 and IL-13. Th2 lymphocytes induce IgE hyperproduction, activation of mast cells, eosinophils, neutrophils and their toxic products. An overexpression of adhesion molecules, RANTES, eotaxin and metalloproteinases contribute to chronic inflammation. A role for substance P and nerve growth factor has been postulated, as well as for other growth factors (epidermal growth factor, fibroblast growth factor and transforming growth factor beta 1) that induce fibroblast growth and new collagen production. Recent studies have also pointed out the role of resident conjunctival cells, such as epithelial cells and fibroblasts, in the inflammatory and remodelling process of vernal keratoconjunctivitis. The pathogenesis of the condition is probably multifactorial, with the interaction of the immune, nervous and endocrine systems.
Vernal keratoconjunctivitis is a chronic inflammatory and potentially blinding disease. Understanding of the complex interactions and cross talk between cells, cytokines and other mediators is relevant for new therapeutic approaches.
本综述旨在描述春季角结膜炎的新免疫病理特征，包括细胞因子、生长因子、细胞、介质和神经递质的参与情况，以及导致组织重塑的机制。
春季角结膜炎是一种影响生活在温暖气候地区年轻男性的过敏性眼病。其特征为结膜巨大乳头、充血以及角膜频繁受累。约50%的春季角结膜炎患者没有特应性疾病的家族史或病史，且未表现出IgE致敏，这表明该疾病并非仅由IgE介导。春季角结膜炎是一种由Th2淋巴细胞驱动的疾病，具有Th2细胞因子衍生模式，IL-3、IL-4、IL-5和IL-13的mRNA水平升高。Th2淋巴细胞诱导IgE过度产生、肥大细胞、嗜酸性粒细胞、中性粒细胞及其毒性产物的激活。黏附分子、RANTES、嗜酸性粒细胞趋化因子和金属蛋白酶的过度表达导致慢性炎症。已推测P物质和神经生长因子以及其他诱导成纤维细胞生长和新胶原产生的生长因子（表皮生长因子、成纤维细胞生长因子和转化生长因子β1）发挥了作用。最近的研究还指出了结膜驻留细胞，如上皮细胞和成纤维细胞，在春季角结膜炎炎症和重塑过程中的作用。该病的发病机制可能是多因素的，涉及免疫、神经和内分泌系统的相互作用。
春季角结膜炎是一种慢性炎症性疾病，有潜在致盲风险。了解细胞、细胞因子和其他介质之间复杂的相互作用和相互影响对于新的治疗方法至关重要。
