Since M. tuberculosis expresses a number of molecules, such as lipoproteins, which activate immune cells in a CD14-dependent manner, we and others investigated whether CD14 also contributed to the host immune response in mice with lung tuberculosis [44] . Although initially after intranasal infection of wild-type and CD14defi cient mice no diff erences in bacterial loads, cell infi ltration and release of most cytokines in the lung were found [44, 45] , at later time points (> 20 weeks after infection) CD14-defi cient mice were protected from mortality presumably as a result of a reduced infl ammatory response in the lungs [44] . Th ese fi ndings are completely opposite to the results from M. tuberculosisinfected TLR2-defi cient and TLR4-mutant mice, which suff ered from reduced bacterial clearance, chronic infl ammation, increased cellular infi ltration of the lungs and reduced survival [46] [47] [48] . Th e mechanism underlying the detrimental eff ect of CD14 in the host response against M. tuberculosis remains to be established.