IRF3 deficiency impacts granzyme B expression and maintenance of memory T cell function in response to viral infection.
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| 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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| Authors | Tyler C Moore, Alexander J Vogel, Thomas M Petro, Deborah M Brown |
| Journal | Microbes and infection (Microbes Infect) Vol. 17 Issue 6 Pg. 426-39 (Jun 2015) ISSN: 1769-714X [Electronic] France |
| PMID | 25777301 (Publication Type: Journal Article, Research Support, N.I.H., Extramural) |
| Copyright | Copyright © 2015 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved. |
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