STAT1 expression controls CD4 T cell Th1 and Th17 effector functionality during influenza virus infection

نویسندگان

چکیده

Abstract Most CD4 T cells primed by influenza A virus (IAV) express the transcription factor T-bet, Th1 ‘master regulator’, and are marked phenotypic functional hallmarks. The extent to which STAT1 STAT4 activation, both needed for maximal T-bet induction in vitro, required direct IAV-primed cell responses is not clear. Here, we transferred STAT-deficient (STAT −/−) or wildtype recognizing IAV congenic mice, challenged them with IAV, analyzed donor infected lungs 7 days later. −/−cells were barely detected host mice but rescued when NK depleted prior infection. Functional analysis revealed compromised identity −/−effectors mirroring that of −/−cells. However, while develop Th17 functions, do not. We show this due alternative receipt type I IFN signals −/−cells, as blocking receptor promotes robust −/−but WT cells. In contrast, −/−donor closely resemble To ask if can respond STAT4-activating treated receiving IL-12 during dramatically increased cytokine production wildtype, −/−or Our findings thus indicate activation sufficient prototypical antiviral effector identity, response fully Th1-polarized without therapeutic activation. This work impacts vaccine strategies aim promote protective immunity against shaping priming environment STAT-activating signals.

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ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2023

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.210.supp.75.48