Immunity enzyme may fight off tuberculosis infection

Immunity enzyme may fight off tuberculosis infection.
Immunity enzyme may fight off tuberculosis infection. | Courtesy of

The University of Texas (UT) Southwestern Medical Center said Tuesday that a recent study by its researchers has revealed how a specific immunity enzyme may protect the body from Mycobacterium tuberculosis (TB) infections.

The enzyme works to protect people against the TB infections that impact million of people around the world and kills approximately 1.5 million people each year.

The study focused on cyclic GMP-AMP synthase (cGAS), an enzyme that is a sensor for the immune system and is crucial to fighting TB. Mice without this enzyme contracted TB much faster than mice with the enzyme.

This new discovery may help scientists create immunity-based therapies to treat TB. Traditional TB treatments require months to adequately fight off the infection. Creating immunity-based therapies may also change how health professionals are dealing with increasingly antibiotic resistant diseases.

"Based on this outcome, we believe that modulating cGAS activity could be a novel approach to therapy. There remains a dire need for new therapies against tuberculosis, and thus identifying pathways to stop the pathogen is of vital importance," Assistant Professor of Internal Medicine and Microbiology at UT Southwestern Michael Shiloh said. Shiloh was co-senior author of the study published in Cell Host & Microbe.

"Tuberculosis is already a significant global pandemic and the threat of multidrug resistance is high. If drug-resistant TB were to spread more internationally, then TB could become a real public health disaster," Shiloh said.

Approximately one-third of the world's population is infected with TB, which is spread by airborne contact.

"The finding that the cGAS pathway is important for sensing and defending against TB infection suggests that this pathway may be harnessed to develop better vaccines and therapeutics to protect people from this dreaded disease," Howard Hughes Medical Institute Investigator and Professor of Molecular Biology Zhijian "James" Chen said.

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University of Texas Southwestern Medical Center

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