New Dual Recognition mechanism discovered in TB
One third of the world’s population is infected with Mycobacterium tuberculosis (MTB), which leads to tuberculosis (TB), a leading cause of death world-wide. A new discovery, led by a team of researchers at the Department of Medicine, offers hope for new approaches to the prevention and treatment of TB.
The team’s discovery of a novel mechanism that may contribute to immune recognition of MTB was published in the September issue of Nature Structural and Molecular Biology.
Building on their 15 years of research together, Clifford V. Harding, MD, PhD, professor and interim chair of pathology, and W. Henry Boom, MD, professor of medicine and director of the Tuberculosis Research Unit found that the potency of LprG, the MTB molecule, to induce immune responses is explained by its combination of two mechanisms to activate Toll-like receptor 2 (TLR2): first, by directly stimulating TLR2 and, second, by serving as a carrier to deliver other molecules that stimulate TLR2. This dual mechanism may drive stronger regulation of immune responses by MTB, and future vaccine development may be enhanced by designing approaches to use such mechanisms.
Furthermore, the work indicates that LprG contributes to the assembly of the bacterial cell wall, suggesting that it may be possible to develop molecules to interfere with LprG function and potentially serve as new antibiotics to fight TB. The development of new antibiotics is an increasingly important goal, since resistance to existing antibiotics is becoming widespread.
