New Hope for Tuberculosis
(Ivanhoe Newswire) – Over two billion people in the world are infected with the bacterium that causes tuberculosis. A new study finds that the presence of a specific molecule allows the immune system to monitor tuberculosis (TB) in the lungs and prevent it from turning into a deadly infection.
The infection is difficult to treat mostly because the bacillus is able to linger in the cells for years without causing symptoms, known as latent TB. When the immune system becomes impaired, the infection becomes active and causes the symptoms, such as night sweats, fever, weight loss, and cough.
"A hallmark of TB that we see on chest X-rays is the granuloma, a collection of immune cells that surround the infected lung cells. But what we didn't know was the difference between a functioning protective granulomae, as in latent TB, and a non-protective granuloma seen in active TB patients. We aimed to find immunologic markers that could show us the status of the infection," Shabaana A. Khader, PhD, senior study author and assistant professor of pediatrics at Pittsburgh School of Medicine, was quoted as saying.
Researchers studied animal models and human TB-infected cells of the disease. They discovered that granulomas that contain ectopic lymphoid structures are associated with suppressing TB effectively. They also found that granulomas that do not contain them are associated with active TB and immune cells, called T-cells, had a surface marker molecule called CXCR5 that is associated with the presence of ectopic lymphoid structures.
"The presence of CXCR5 provides a specific address for the infected cells that tells the immune cells where to focus their attention to contain the problem. That results in the formation of ectopic lymphoid structures and the protective granuloma that keeps TB infection under control, unlike in active disease. Without CXCR5, those structures did not form and active TB was more likely,” Dr. Khader explained.
The researchers delivered CXCR5 T-cells from donor animals to TB-infected mice that lacked CXCR5, which resulted in T-cell localization and ectopic lymphoid structure formation was restored leading to a decrease in susceptibility to TB.
"The protective power of CXCR5 points us in a novel direction for future management of TB. These findings have powerful implications for the development of vaccines to prevent infection,” Dr. Khader concluded.
Source: Journal of Clinical Investigation, January 2013