We show that absence of both IL-1α plus IL-1β recapitulated the overwhelming infection and acute necrotic pneumonia seen in IL-1R1 deficient mice, while presence of either IL-1α or IL-1β allowed to control acute M. tuberculosis infection and pulmonary inflammation, with limited lung infiltration of inflammatory cells, oedema and necrosis. The gene discussed is IL1A; the disease is pneumonia.