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Bussmeyer U et al. – Molecular analyses revealed that, compared to uninfected PMN, A. phagocytophilum decreased the expression of the IFN–gamma receptor alpha–chain CD119, diminished the IFN–gamma–induced phosphorylation of STAT1, and enhanced the expression of SOCS1 and SOCS3 in PMN. Since IFN–gamma activates various antibacterial effector mechanisms of PMN, the impaired IFN–gamma signaling in infected cells likely contributes to the survival of A. phagocytophilum inside PMN and to HGA disease development.


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