Dual Recognition Mechanism in TB

Dual Recognition Mechanism in TB

Researchers at Case Western Reserve University School of Medicine have gained new insight into how tuberculosis evades the body's immune system, offering hope for new approaches to treatment and prevention.

One-third of the world's population is infected with the bacteria that causes most cases of tuberculosis: Mycrobacterium tuberculosis (MTB). While most people recover from TB infection, the bacteria can lie dormant, hiding in the body's own immune cells for years before reactivating and causing serious illness or even death.

A recent study indicates that MTB can inhibit the ability of immune cells called macrophages to fight infection, and the researchers have identified a protein called LprG, which is expressed by MTB. LprG signals through the macrophage protein Toll-like receptor 2 (TLR2) to regulate macrophage functions, resulting in changes that help the bacteria to evade the immune system.

LprG seems to be able to manipulate the body's immune system first by directly stimulating the TLR2 and second by delivering other molecules to do the same. Too much stimulation of TLR2 causes some parts of the immune system to shut down, according to Clifford V. Harding, MD, PhD, chair of the school's pathology department.

A better understanding of MTB's interaction with the immune system is essential to designing new TB vaccines.