Mycobacterium tuberculosis senses host Interferon-γ via the membrane protein MmpL10

Tuberculosis (TB) is a serious infectious disease caused by a bacterium called Mycobacterium tuberculosis (Mtb). When the body’s immune system recognizes the presence of the bacteria, it produces a protein called Interferon-γ (IFN-γ), which plays a crucial role in fighting the infection. Specifically, IFN-γ regulates the activity of immune cells that are involved in killing Mtb and thereby control infection.

In this research study, Al Leslie and colleagues investigated how in addition to directing host immunity, IFN-γ might also have an effect on Mtb. They discovered that a membrane protein in the bacteria, known as mycobacterial membrane protein large 10 (MmpL10), plays a vital role in this process. MmpL10 acts like a sensor, allowing the bacterium to detect the presence of IFN-γ. Once the Mtb senses the presence of IFN-γ, they respond by altering their behaviour, such as increasing their metabolism, potentially becoming more virulent or adapting their survival strategies to counter the host’s immune defenses.

Understanding how Mtb interacts with the human immune system is crucial for developing effective treatments for TB. By identifying the role of MmpL10 in sensing IFN-γ, researchers have opened up new avenues for developing targeted therapies to disrupt this communication and potentially weaken the ability of Mtb to cause harm.

Ultimately, this research brings us one step closer to developing more precise and efficient strategies for combating TB  and offers hope for improved treatments and control of this most challenging infectious disease.