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Francisella infection up-regulates SOCS3 expression, which suppresses STAT1 phosphorylation potentially by binding to the IFNγ receptor and dampening subsequent recruitment and activation of STAT1. Ultimately, Francisella-mediated suppression of the IFNγ response leads to the inhibition of IFNγ-induced iNOS and other anti-microbial events, resulting in enhanced bacterial survival in host cells.
