IRF3 deficiency impacts granzyme B expression and maintenance of memory T cell function in response to viral infection

Microbes and Infection
Tyler C MooreDeborah M Brown

Abstract

The role of interferon regulatory factor 3 (IRF3) in the innate immune response to infection has been well studied. However, less is known about IRF3 signaling in shaping the adaptive T cell response. To determine the role of IRF3 in the generation and maintenance of effective anti-viral T cell responses, mice deficient in IRF3 were infected with a potentially persistent virus, Theiler's murine encephalomyelitis virus (TMEV) or with a model acute infection, influenza A virus (IAV). IRF3 was required to prevent TMEV persistence and induce robust TMEV specific effector T cell responses at the site of infection. This defect was more pronounced in the memory phase with an apparent lack of TMEV-specific memory T cells expressing granzyme B (GrB) in IRF3 deficient mice. In contrast, IRF3 had no effect on antigen specific T cell responses at the effector stage during IAV infection. However, memory T cell responses to IAV were also impaired in IRF3 deficient mice. Furthermore, addition of cytokines during peptide restimulation could not restore GrB expression in IRF3 deficient memory T cells. Taken together, IRF3 plays an important role in the maintenance of effective anti-viral T cell memory responses.

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Citations

Mar 26, 2016·Frontiers in Immunology·Deborah M BrownAspen M Workman
Sep 20, 2016·Cellular Immunology·Zacharey GuinnThomas M Petro
Jun 27, 2017·International Immunopharmacology·Zachary GuinnThomas M Petro
Nov 20, 2018·The Journal of General Virology·Kimberly L W SchultzDiane E Griffin
Feb 9, 2017·Frontiers in Immunology·Jennifer A JunoC Mee Ling Munier
Jan 24, 2019·International Journal of Molecular Sciences·Ingo GerhauserAndreas Beineke
Oct 7, 2020·The Journal of Immunology : Official Journal of the American Association of Immunologists·Thomas M Petro

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