Although the etiology of Mooren's ulcer is poorly understood, recent evidence suggests that the pathogenesis of this disease appears to be the result of an autoimmune process directed against molecules expressed in the corneal stroma.
[citation needed] Previous ocular trauma or infection can cause disruption of the corneal integrity resulting in the expression of tissue-specific antigens that are normally hidden from the immune system.
[7] Immunohistochemical studies in patients suffered from Mooren's ulcer showed massive infiltration of multiple types of inflammatory cells in the conjunctival tissue.
The cell types in the inflammatory lesion includes CD4+ and CD8+ T-lymphocytes, B-lymphocytes, macrophages, a small amount of neutrophils was also observed in the conjunctiva from patients with Mooren's ulcer.
[10] Gottsch and colleagues have suggested that calgranulin C, a protein expressed in the corneal stroma, may be a possible main target for autoimmune response causing Mooren’s ulcer.
[11] Also, significantly increased expression levels of adhesion and co-stimulatory molecules have been found in ocular tissues affected by Mooren's ulcer compared to healthy eyes.
Several case reports showed that biological agents, such as anti-tumor necrosis factor alpha (anti-TNF) or monoclonal antibodies against CD20, also can be used as an effective treatment of progressive Mooren’s ulceration.
In addition, the amniotic membrane contains a large number of collagens, growth factors and protease inhibitors which can promote healing and reconstruction of the conjunctival epithelium.