Cytokines in posterior uveitis: An update

T helper (Th) lymphocytes differentiate into two distinct subsets - Th1 and Th2 - as defined by functional abilities and cytokine profiles. The functional differences between Th subsets are explained primarily through the activities of the cytokines they secrete. Interferon-γ (IFN-γ) is the signature cytokine of Th1 cells, which also produce interleukin-2 (IL-2) and tumor necrosis factor-β (TNF-β). IL-4 is the corresponding signature cytokine of Th2 cells, which also secrete IL-5, IL-6, IL-9, and IL-13. Recently, a few transcription factors have been identified that not only control the expression of cytokines of a particular type but also repress cytokines of other types. Human Th1 and Th2 cells not only produce a different set of cytokines but also exhibit distinct functional properties and the preferential expression of some activation markers. Pathophysiologically, the two subsets have been found to be mutually antagonistic. Various Th1 and Th2 cytokines appear to play an important role in the etiopathogenesis of posterior uveitis and its animal model, experimental autoimmune uveitis (EAU). The exact contribution of these mediators to uveitis remains to be defined. Recent studies suggest that a shift from Th1- to Th2-dominated response could be of therapeutic benefit. This review evaluates various studies in which uveitopathogenic and therapeutic potentials of various Th1 and Th2 cytokines have been investigated.