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- Title
IRF4 and BATF are critical for CD8<sup>+</sup> T-cell function following infection with LCMV.
- Authors
Grusdat, M; McIlwain, D R; Xu, H C; Pozdeev, V I; Knievel, J; Crome, S Q; Robert-Tissot, C; Dress, R J; Pandyra, A A; Speiser, D E; Lang, E; Maney, S K; Elford, A R; Hamilton, S R; Scheu, S; Pfeffer, K; Bode, J; Mittrücker, H-W; Lohoff, M; Huber, M
- Abstract
CD8+ T-cell functions are critical for preventing chronic viral infections by eliminating infected cells. For healthy immune responses, beneficial destruction of infected cells must be balanced against immunopathology resulting from collateral damage to tissues. These processes are regulated by factors controlling CD8+ T-cell function, which are still incompletely understood. Here, we show that the interferon regulatory factor 4 (IRF4) and its cooperating binding partner B-cell-activating transcription factor (BATF) are necessary for sustained CD8+ T-cell effector function. Although Irf4-/- CD8+ T cells were initially capable of proliferation, IRF4 deficiency resulted in limited CD8+ T-cell responses after infection with the lymphocytic choriomeningitis virus. Consequently, Irf4-/- mice established chronic infections, but were protected from fatal immunopathology. Absence of BATF also resulted in reduced CD8+ T-cell function, limited immunopathology, and promotion of viral persistence. These data identify the transcription factors IRF4 and BATF as major regulators of antiviral cytotoxic T-cell immunity.
- Subjects
LYMPHOCYTIC choriomeningitis virus; ANTINEOPLASTIC agents; ANTIVIRAL agents; CLINICAL immunology; CELL physiology; ARENAVIRUS diseases; TRANSCRIPTION factors
- Publication
Cell Death & Differentiation, 2014, Vol 21, Issue 7, p1050
- ISSN
1350-9047
- Publication type
Article
- DOI
10.1038/cdd.2014.19