In these experiments, the infecting dose determined using lungs collected from control C57BL/6 mice (n = 5) immediately following challenge is 4.26 ± 0.28 log CFU/mouse, which is consistent with a previous report (Kahl-McDonagh et al., 2007) . Bacterial load recovered from the lungs of TLR2 −/− , TLR4 −/− , and MyD88 −/− mice during the first two weeks following exposure is not significantly different from the C57BL/6 control mice (Figure 1 , panels W1-2), indicating that TLR2, TLR4, and MyD88 are not required to clear lung infection early. A significant difference in bacterial burden is detectable by week 4 and extends through week 10, indicating that the contribution of TLR2, TLR4, and MyD88 to the control of Brucella infection in the lungs occurs via adaptive immunity (Figure 1 ). By week 4 p.i., there was a significant difference in the clearance of the organism from each of the knockouts. This pattern persisted through week 10, although significance is lost due to the reduction in the number of animals available at this time point. The absence of MyD88 appears to have a greater impact on the clearance of infection from the lungs over this period, as the bacterial burden in the lungs of MyD88 −/− mice is significantly higher than that in TLR2 −/− and TLR4 −/− mice by week 8 p.i. (Figure 1, panel W8 ). The kinetics of Brucella clearance from the lungs is summarized in Figure 1K , and taken together, these results indicate that TLR2, TLR4, and MyD88 contribute to Brucella clearance from the lungs following aerosol challenge.