Abstract
The blinding inflammatory lesion stromal keratitis (SK), which occurs in some patients in response to ocular herpes simplex virus (HSV) infection, represents mainly an immune cell mediated inflammatory response to the virus infection. The principal orchestrators of the immunopathological lesions are T cells although additional events participate that include the extent of recruitment of non-lymphoid cells, the extent of neoangiogenesis, and the extent of damage to nerve function. This review focuses on evidence that the balance of the functional subsets of T cells has a major impact on lesion severity and duration. Accordingly, if proinflammatory Th1 and Th17 CD4 T cells, and perhaps in some cases CD8 T cells, predominate lesions occur earlier and are more severe. Lesions are diminished when cells with regulatory function predominate. Moreover, when regulatory cells acquire the property to produce Amphiregulin this may facilitate lesion resolution. An objective to controlling lesions is to learn how to manipulate the balance of T cells to favor the representation and function of regulatory T cells and their products over proinflammatory cells. In this review we emphasize how exploiting the differential metabolic requirements of immune cells could be a valuable approach to control SK.