Corneal stromal keratocytes contribute to the maintenance of corneal transparency and shape by synthesizing and degrading extracellular matrix. They are quiescent in the healthy cornea, but they become activated in response to insults from the external environment that breach the corneal epithelium, with such activation being associated with phenotypic transformation into fibroblasts. Corneal fibroblasts (activated keratocytes) act as sentinel cells to sense various external stimuli—including damage-associated molecular patterns derived from injured cells, pathogen-associated molecular patterns of infectious microorganisms, and inflammatory mediators such as cytokines—under pathological conditions such as trauma, infection, and allergy. The expression of various chemokines and adhesion molecules by corneal fibroblasts determines the selective recruitment and activation of inflammatory cells in a manner dependent on the type of insult. In infectious keratitis, the interaction of corneal fibroblasts with various components of microbes and with cytokines derived from infiltrated inflammatory cells results in excessive degradation of stromal collagen and consequent corneal ulceration. Corneal fibroblasts distinguish between type 1 and type 2 inflammation through recognition of corresponding cytokines, with their activation by type 2 cytokines contributing to the pathogenesis of corneal lesions in severe ocular allergic diseases. Pharmacological targeting of corneal fibroblast function is thus a potential novel therapeutic approach to prevention of excessive corneal stromal inflammation, damage, and scarring.

角膜基质角膜细胞通过合成和降解细胞外基质，有助于维持角膜透明性和形状。它们在健康的角膜中是静止的，但是它们响应于突破角膜上皮的外部环境的伤害而被激活，这种激活与表型转化为成纤维细胞有关。角膜成纤维细胞（活化的角膜细胞）充当哨兵细胞，可在病理条件下（例如创伤，疾病或其他疾病）感应各种外部刺激，包括损伤细胞的损伤相关分子模式，传染性微生物的病原体相关分子模式以及细胞因子等炎性介质。感染和过敏。角膜成纤维细胞表达的各种趋化因子和粘附分子决定了炎症细胞的选择性募集和活化，其方式取决于损伤的类型。在传染性角膜炎中，角膜成纤维细胞与微生物的各种成分以及与由渗透的炎性细胞衍生的细胞因子的相互作用导致基质胶原过度降解并因此导致角膜溃疡。角膜成纤维细胞通过识别相应的细胞因子来区分1型和2型炎症，其被2型细胞因子激活导致严重的眼部过敏性疾病的角膜病变。