Accordingly, reduced uptake by macrophages could be one of a multitude of events that contribute to resistance against TB. This conclusion is supported by an experiment showing that a depletion of alveolar macrophages increased resistance to tuberculosis in a murine infection model indicating that uptake by macrophages serves the survival and propagation of the mycobacteria rather than their control by the host. The observations made in this mouse model are, however, not directly valid in human disease. As MBL bound less effectively to M. tuberculosis in vitro one may also hypothesize that impairment of MBL function is of less relevance in TB caused by lineages of this species. Since MBL is only one of several components which interact with mycobacterial surface moieties, other mediators and cellular receptors might be more important in the phagocytic uptake of M. tuberculosis. In addition to MBL, the mannose receptor of macrophages as well as receptors for complement, surfactant protein A, macrophage scavenger receptors and CD14 all have been reported to be involved in PD 168,077 maleate salt pathogen-macrophage interactions. Thus, alternative mechanisms of uptake of mycobacteria by macrophages exist and the responsiveness of macrophages does not exclusively depend on recognition of mycobacterial structures by MBL. It may, therefore, be concluded that some or all of these receptors are more relevant in M. tuberculosis than in M. africanum/M. bovis infections. Genome analyses of several MTBC phylogenetic lineages have CP-863187 revealed a multitude of variations indicating that the members of the MTBC are far more genetically diverse than previously thought. Genes of various functional categories such as those encoding constituents of metabolic pathways, membrane proteins and virulence factors show remarkable variability, and the various lineages are characterized by deep-tailed genomic deletions. So far, the effect of genetic variation on the composition of cell walls of M. africanum/M. bovis and M. tuberculosis is incompletely explored. In particular, it is not clear whether the RD9 deletion, which is characteristic for M. africanum lineages and for M. bovis, has an influence on the composition of cell surface structures which might be relevant to MBL binding. The binding characteristics of MBL to microbes are also not fully understood.