IFNA1 and infection: While STAT2 deficiency alone did not affect Brucella burdens, a combined deficiency of STAT2 and the IFN-γ receptor led to elevated Brucella burdens in brains and blood, and a higher likelihood of developing neurologic symptoms relative to animals lacking the IFN-γ receptor alone.<h4>Conclusions</h4>Our findings indicate that T cells and IFN signaling through both STAT1 and STAT2 play complex and important roles in protecting against bacterial colonization and development of neurologic symptoms following infection by Brucella.