These findings suggest that type I IFN signaling contributes substantially to the pro-inflammatory neutrophil response in TB-susceptible C3HeB/FeJ mice, including the elevation of pro-inflammatory chemokines Ccl3, Ccl4, and Cxcl2, as well as limited expression of the effector T cell–attractant chemokine Cxcl9 observed during disease progression in these mice, in accordance with the improved CD4+ T cell accumulation in TB lesions observed with IFNAR blockade. The gene discussed is IFNAR1; the disease is tuberculosis.