We found that CXCL9, CXCL10, and CXCL11 each exert direct antimicrobial effects against B. anthracis in vitro and that neutralization of endogenous CXCL9, individually or together with CXCL10 or CXCL10/CXCL11, but not CXCR3, significantly increases host susceptibility to inhalational anthrax in a murine model of infection. This evidence concerns the gene CXCR3 and anthrax infection.