Utilization of CD11b knockout mice to characterize the role of complement receptor 3 (CR3, CD11b/CD18) in the growth of Mycobacterium tuberculosis in macrophages

Using CD11b knockout mice as a source of macrophages (M phi), 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 M phi. We demonstrate that opsonic binding of M. tuberculosis to M phi is mediated by an immunoglobulin-independent, heatlabile component of serum, in both the presence and the absence of CD11b. The survival and replication of M. tuberculosis in an in vitro M phi 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 M phi that the bacterium enters, is significantly affected by the presence or absence of CR3. (C) 2000 Academic Press.