Abstract
Abstract: :
Purpose: Following HSV–1 corneal infection, the virus establishes a latent infection in the sensory ganglia. Reactivation of latent virus in sensory neurons, and transport down nerve axons serves as a source of virus for recurrent disease at the periphery. We have observed that a population of HSV–1 specific memory CD8+ T cells remains in the ganglia during viral latency and can directly monitor HSV–1 gene expression in sensory neurons, and block HSV–1 reactivation from latency. The purpose of this study was to determine the requirement for the cytokines IL–2 and IL–15 in maintaining this population of memory CD8 T cells in the infected ganglia Methods: Infection of IL–15 knockout mice and/or mice treated with antibody to neutralizate IL–2 followed by evaluation of CD8 T cell numbers, antigen specificity, and activation phenotype in the trigeminal ganglion (TG) and draining lymph nodes (DLN) determined cytokine involvement. Results: In the DLN, neither IL–15 nor IL–2 was required for expansion of HSV–specific CD8 T cells, but IL–15 was required for expansion of non–specific CD8 T cells. In the TG, both IL–2 and IL–15 were required for the expansion of HSV–specific and non–specific memory CD8 T cells, while only IL–15 was required for homeostasis Conclusions: IL–2 and IL–15 play important, non–redundant roles in maintaining a pool of virus–specific and non–specific memory CD8 T cells during latent virus infections.
Keywords: cytokines/chemokines • herpes simplex virus • immunomodulation/immunoregulation