TB study reveals how the bacterium hijacks part of the immune system meant to protect against infection. Scientists from the University of Cape Town have helped uncover a key reason why tuberculosis (TB) remains so effective at infecting humans and animals. The bacterium responsible is able to hijack part of the immune system designed to protect the body from disease.
The international study found thatMycobacterium tuberculosis(MTB) exploits an immune receptor known as Dectin-1 — normally crucial in fighting fungal infections, to survive and multiply inside host cells. The findings were published in Science Immunology. (MTB) exploits an immune receptor known as Dectin-1 — normally crucial in fighting fungal infections, to survive and multiply inside host cells.
Despite more than a century of research, TB remains one of the world’s deadliest bacterial infections, causing an estimated 1.5 million deaths each year. TB infection begins when airborne bacteria are inhaled and engulfed by immune cells such as macrophages. These cells rely on surface receptors to recognise invading microbes and trigger protective immune responses.
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One such receptor, Dectin-1, is best known for its role in anti-fungal immunity. However, the researchers found that MTB has evolved to turn this defence mechanism to its advantage. The study showed that MTB targets Dectin-1 to drive immune responses that favour bacterial survival rather than clearance.
When the Dectin-1 pathway was absent, both human and mouse cells were better able to control TB infection. Mice lacking the receptor were significantly more resistant to the disease.
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