Figure 9

Ocular surface immuno-inflammatory status in KC: (a) The schematic represents the immune cell subtypes on the ocular surface of KC patients (across different grades of the disease) that were significantly different increased or decreased compared to controls. The schematic also indicates the various tear fluid soluble factors whose levels were significantly altered in KC (across different grades of the disease) compared to controls. (b) Represents the hypothetical immuno-inflammatory amplification cycle in keratoconus pathogenesis. External stimuli including physical and/or biological stimuli, oxidative stress, eye rubbing, etc., can stimulate the corneal structural cells such as the epithelium and keratocytes to secrete various active biologically active factors, including those with inflammatory and chemoattract properties. This will facilitate the recruitment and activation of immune cells on the ocular surface. The activation of immune cells might result in additional secretion of immune- and inflammatory mediators which can adversely impact the homeostasis and function of the corneal structural cells. This can result in aberrant extra-cellular matrix (ECM) remodeling due to decreased collagen synthesis, reduction in endogenous cross-linking enzyme and increased degradation of ECM proteins via proteases. Thus, causing structural and biomechanical changes characteristics of KC. The function of corneal epithelium and keratocytes will further be influenced by changes in the biophysical cues due to altered ECM remodeling, thus contributing to disease progression in KC.