Mooren’s ulcer, a relatively uncommon painful peripheral corneal ulceration without associated scleral involvement deserves a special mention in this regard. Although there are sufficient evidences to suggest the autoimmune nature of the disease, the precise pathophysiological mechanism remains unclear. High levels of proteolytic enzymes have been demonstrated in the affected conjunctiva [11]. Foster and colleagues had established the presence of numerous activated neutrophils in the affected cornea and eventually proposed that these neutrophils were the source of proteolytic enzymes [12]. Researchers also noted that systemically, helper T cells outnumbered supressor T cells in patients with Mooren’s ulcer. It was proposed that unregulated helper T cells could induce production of autoantibodies, resulting in deposition of immune complexes, complement activation followed by inflammatory cell infiltration and release of proteolytic enzymes [13, 14].

However, it is important to remember that inflammatory involvement of adjacent conjunctiva, episclera, and sclera is not a feature of all types of PUK. A simple hypersensitivity reaction to exogenous antigens may induce marginal keratitis and phlyctenular keratitis in the peripheral cornea that has an excellent prognosis when compared to immune diseases-related PUK.