The Nrf2 activator, tBHQ, blunts dendritic cell function upon influenza A infection 9080

Abstract Description Dendritic cells (DCs) are critical for linking innate and adaptive immunity by activating T cells through antigen presentation via MHCII. Previous research from our lab revealed that tert-butylhydroquinone (tBHQ), a common food additive and Nrf2 activator, impairs CD8+ T cell activation and effector function, though the mechanism remains unclear. Since DCs are pivotal in T cell activation, we hypothesized that tBHQ exposure inhibits DC maturation and activation during influenza A infection. To test this, female C57BL/6 mice were fed either a control (0% tBHQ) or standard (0.0014% tBHQ) AIN-93G diet for two weeks before infection with influenza A virus (A/PR/8/34). Lung and mediastinal lymph node (MLN) DCs were collected post-infection and analyzed by flow cytometry. tBHQ significantly reduced DC maturation (decreased MHCII expression) and activation (reduced expression of CD40, CD80/86). Additionally, DCs from tBHQ-fed mice showed lower production of key cytokines, IL-6 and IL-12. These results suggest that tBHQ exposure impairs DC function, potentially disrupting T cell activation and weakening immune responses to viral infections. This study raises concerns about tBHQ’s immunosuppressive effects and its broader implications for immune defense, particularly in the context of respiratory infections. Funding Sources Supported by NIH R01 ES024966 and NIH R21 ES033830. Topic Categories Immune Mechanisms of Human Disease (HUM)