Kris Huygen and colleagues, at the Scientific Institute of Public Health, Belgium, have now identified a role for LXR proteins in the mouse immune response to airway infection with Mycobacterium tuberculosis, the bacterium that causes tuberculosis.
As treatment of normal mice with molecules that activate LXRs provided substantial protection from both a new infection and established infections, the authors suggest that LXRs might provide a new target for tuberculosis therapeutics.
In the study, when compared with normal mice, mice lacking both forms of LXR (LXR-alpha and LXR-beta) were more susceptible to airway infection with Mycobacterium tuberculosis
and developed more severe disease.
Further analysis revealed that these mice did not mount an effective immune response in the airways. For example, there was no accumulation of immune cells known as neutrophils in the lungs and little evidence of Th1 and Th17 immune responses.
Importantly, the marked protection from infection seen in normal mice treated with molecules that target LXRs was accompanied by increased Th1 and Th17 immune responses.