gms | German Medical Science

Since the cornea is devoid of blood and lymphatic vessels, the relationship between de novo corneal heme- and lymphangiogenesis, both at the mechanistic level, as well as their differential contribution to immune and inflammatory responses in the cornea and anterior segment, have been the subject of much study and debate over the last few decades. The identification of critical molecular mediators, as well as inhibitors, of vasculogenesis has allowed this field to progress rapidly over the past decade. Within the eye field, application of new tools and reagents to rodent models of corneal inflammation and immunity, in particular transplantation, has allowed us to understand better than ever before the codependence of these two processes, as well as how they differ. The current paradigm with which we are currently working proposes that while heme- and lymphangiogenesis are induced by similar inflammatory stimuli (e.g., cytokines such as IL-1), they are distinct in the following ways: 1) they are mediated, in part, by ligation of distinct receptors, 2) they differentially contribute to innate immunity, and 3) to the afferent vs. effector arm of adaptive antigen-specific immunity. Dissection of the molecular mechanisms that mediate heme- and lymphangiogenesis will aid not only in a better understanding of ocular pathophysiology and immunology, but also in devising novel targeted molecular strategies that could modulate distinct aspects of these two vasculogenic processes.