Down-Ranking the Threat of HSV-1: RANKL Upregulates MHC Class I Restricted Anti-Viral Immunity in Herpes Simplex Virus Infection

    Katja Finsterbusch, Vincent Piguet
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    TLDR RANKL improves the immune response against herpes simplex virus by enhancing T cell activation and could help develop better treatments or vaccines.
    The document describes a study by Klenner and colleagues from 2015, which demonstrated that the receptor activator of NFKB ligand (RANKL) is critical for the immune response against Herpes Simplex Virus type 1 (HSV-1). RANKL was found to be essential for the induction of anti-viral CD8+ effector T cells in cutaneous HSV-1 infection. It prevents apoptosis in Langerhans cells, enhances antigen transport to lymph nodes, and increases the CTL-priming capacity of dendritic cells in lymph nodes. These findings suggest that RANKL could be a potential target for improving anti-viral immunity against HSV-1 and may contribute to the development of new vaccines or therapies. However, the document does not provide the number of subjects in the study, which is necessary to determine the study's strength.
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