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Article Dans Une Revue Journal of Experimental Medicine Année : 2020

β2-adrenergic signals downregulate the innate immune response and reduce host resistance to viral infection

Résumé

In humans, psychological stress has been associated with a higher risk of infectious illness. However, the mechanisms by which the stress pathway interferes with host response to pathogens remain unclear. We demonstrate here a role for the β2-adrenergic receptor (β2-AR), which binds the stress mediators adrenaline and noradrenaline, in modulating host response to mouse cytomegalovirus (MCMV) infection. Mice treated with a β2-AR agonist were more susceptible to MCMV infection. By contrast, β2-AR deficiency resulted in a better clearance of the virus, less tissue damage, and greater resistance to MCMV. Mechanistically, we found a correlation between higher levels of IFN-γ production by liver natural killer (NK) cells and stronger resistance to MCMV. However, the control of NK cell IFN-γ production was not cell intrinsic, revealing a cell-extrinsic downregulation of the antiviral NK cell response by adrenergic neuroendocrine signals. This pathway reduces host immune defense, suggesting that the blockade of the β2-AR signaling could be used to increase resistance to infectious diseases.
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hal-02982518 , version 1 (02-11-2020)

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Elisabeth Wieduwild, Mathilde Girard-Madoux, Linda Quatrini, Caroline Laprie, Lionel Chasson, et al.. β2-adrenergic signals downregulate the innate immune response and reduce host resistance to viral infection. Journal of Experimental Medicine, 2020, 217 (4), ⟨10.1084/jem.20190554⟩. ⟨hal-02982518⟩
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