Utilization of CD11b Knockout Mice to Characterize the Role of Complement Receptor 3 (CR3, CD11b/CD18) in the Growth of Mycobacterium tuberculosis in Macrophages

Abstract

Using CD11b knockout mice as a source of macrophages (Mφ), we show that complement receptor 3 (CR3) mediates approximately 40–50% of nonopsonic binding and 50–60% of serum-mediated binding of Mycobacterium tuberculosis to resident Mφ. We demonstrate that opsonic binding of M. tuberculosis to Mφ is mediated by an immunoglobulin-independent, heat-labile component of serum, in both the presence and the absence of CD11b. The survival and replication of M. tuberculosis in an in vitro Mφ model and an in vivo mouse model of infection were not significantly affected by the absence of CD11b, indicating that CR3-mediated uptake of M. tuberculosis is not a major factor in controlling the subsequent intracellular survival of the mycobacteria. However, whether a mycobacterium will gain access to the intracellular environment, and the type of Mφ that the bacterium enters, is significantly affected by the presence or absence of CR3.