Figure 1: Model of immune mechanisms of TLR2-mediated control of an anti-HSV-1 immune response in the conjunctiva. During topical ocular immunization with TLR2 agonist (1), high concentration of exogenous TLR2 agonist is sensed by conjunctiva APC and Treg cells residing in the epithelium and then triggers the migration of conjunctiva resident APC (DC) and Treg to the proximal draining lymph node (2, 4) or (dashed arrow) to the conjunctiva lymphoid follicles (CLF). TLR2/TLR2L interaction promotes maturation of DC and proliferation of Tregs paralleled by temporarily abrogated suppression (empty arrow). As a result, Tregs do not suppress the ongoing immune response in the draining lymph node or in CLF. (3) DC stimulate naïve CD4+ and CD8+ effector T cells which undergo cell division and proliferation in the draining LN (5) or CLF where they form with B cells a germinal center (characteristic of lymphoid follicles). Activated effector T cells migrate to the epithelium and kill HSV-1-infected epithelial cells through CTL activity. Some activated effector cells in the LN preferentially migrate to the periphery through lymphoid afferent canal to induce systemic immune response. Once HSV-1 is cleared by the immune system and the source of TLR2 ligands is no longer present, Tregs will regain their suppressive capabilities, thus contributing to the balance between tolerance and immunity.