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Mycobacterium tuberculosis Infection in Complement Receptor 3-Deficient Mice¹

Chenggang Hu^*, Tanya Mayadas-Norton, Katie Tanaka, John Chan^§ and Padmini Salgame^2,*

^* Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140; Department of Pathology, Harvard Medical School, Boston, MA 02115; and Departments of Pathology and ^§ Medicine, Montefiore Medical Center, Bronx, NY 10461

Complement receptor type 3 (CR3) present on macrophages is used by Mycobacterium tuberculosis as one of its major phagocytic receptors. In this study, we examined the in vivo significance of CR3-mediated phagocytosis on the pathogenesis of disease caused by M. tuberculosis. The outcome of tuberculous infection in mice deficient in the CD11b subunit of CR3 (CR3^-/-) on a mixed 129SV and C57BL background and control wild-type counterparts was comparable with respect to survival, bacterial burden, granulomatous lesion development, and cytokine expression in the spleen and lungs. M. tuberculosis infection was also examined in CR3^-/- mice on C57BL/6 and BALB/c backgrounds 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 relatively resistant C57BL/6 or the relatively susceptible BALB/c strains of mice.

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