Tuberculosis remains one of the world's most devastating infectious diseases, second only to HIV and AIDS. While medicine has made significant in-roads in the fight against the illness, Nature reports that drug-resistant forms of tuberculosis have pose a larger problem than ever. Even without considering the drug-resistant forms of tuberculosis, an estimated third of the global population is infected with Mycobacterium tuberculosis at any given moment; 1.4 million people died of tuberculosis in 2011 alone. However, the majority of people infected with the disease will live with no symptoms and die of other causes. Researchers from the University of Pittsburgh believe that they have discovered why, and hope that their finding will lead to a new, more potent vaccine.

A study published in the Journal of Clinical Investigation examines the roots of latent tuberculosis. Part of the reason that the disease is so difficult to treat is that though many people have no symptoms for years, about 10 percent of people with latent tuberculosis develop an active infection. The bacteria will enter the person's cells and then, when the immune system becomes impaired from old age or another infection, like HIV, the disease rears its head, causing the characteristic cough, night sweats and weight loss.

The researchers studied human cells and animal models of the disease. They found that the ectopic lymphoid structure, which resembles lymph nodes, can single-handedly mean the difference between an active and a latent TB infection. Immune cells carry a molecule called CXCR5, which is the marker for the presence of the ectopic lymphoid structure. In TB patients, granulomas, collections of immune cells, gather around the infected lung cells. In patients who have granulomas that contain the ectopic lymphoid structure, the body is able to suppress the disease. In patients without the ectopic lymphoid structure, the tuberculosis infection becomes active.

"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," Shabaana Kader, the study's senior author, explained in a statement. "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...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."