Mycobacterium tuberculosis infection in complement receptor 3-deficient mice

Complement receptor type 3 (CR3) present on macrophages Is used by Mycobact erium tuberculosis as one of its major phagocytic receptors, In this study, we examined the in vivo significance of CR3-mediated phagocytosis on the p athogenesis of disease caused by M. tuberculosis. The outcome of tuberculou s infection in mice deficient in the CD11b subunit of CR3 (CR3(-/-)) on a m ixed 129SV and C57BL background and control wild-type counterparts was comp arable with respect to survival, bacterial burden, granulomatous lesion dev elopment, and cytokine expression in the spleen and lungs. M. tuberculosis infection was also examined in CR3(-/-) mice on C57BL/6 and BALB/c backgrou nds and was found to be similar, In conclusion, our results suggest that in the absence of CR3, M. tuberculosis is able to gain entry into host cells via alternative phagocytic receptors and establish infection. The data also indicate that absence of CR3 does not alter disease course in either the r elatively resistant C57BL/6 or the relatively susceptible BALB/c strains of mice.