Double-knockout (KO) mice, deficient in both IL-1α and IL-1β, following infection with M. tuberculosis H37Rv, have been reported to develop larger granulomatous lesions (Yamada et al., 2000), whereas IL-1 type 1 receptor knockout mice were highly susceptible, showed greater mycobacterial load, and developed granulomas with fewer MΦs and lymphocytes, and abundant granulocytes (Juffermans et al., 2000). This evidence concerns the gene IL1A and infection.