Home  |  Top News  |  Most Popular  |  Video  |  Multimedia  |  News Feeds  |  Feedback
  Medicine  |  Nature & Earth  |  Biology  |  Technology & Engineering  |  Space & Planetary  |  Psychology  |  Physics & Chemistry  |  Economics  |  Archaeology
Top > Medicine, Health Care > Pitt-led Team Finds Molecule That… >

Pitt-led Team Finds Molecule That Polices TB Lung Infection, Could Lead to Vaccine

Published: January 2, 2013.
Released by University of Pittsburgh Schools of the Health Sciences  

PITTSBURGH, Jan. 2, 2013 – The presence of a certain molecule allows the immune system to effectively police tuberculosis (TB) of the lungs and prevent it from turning into an active and deadly infection, according to a new study led by researchers at Children's Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. Their findings appear today in the online version of the Journal of Clinical Investigation.

More than 2 billion people or one-third of the world's population are infected with mycobacterium tuberculosis, the bacterium that causes TB, said senior author Shabaana A. Khader, Ph.D., assistant professor of pediatrics, Pitt School of Medicine. The infection is challenging to treat partly because the bacillus is able to enter cells and linger for years without causing symptoms, known as latent TB. Then, typically when the immune system becomes impaired due to other reasons such as age or HIV, the infection becomes active and causes the cough, night sweats, fever and weight loss that characterize the disease.

"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," Dr. Khader said. "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."

For the study, which was funded by the National Institutes of Health, the researchers studied human TB-infected cells as well animal models of the disease. They found that granulomas that contain ectopic lymphoid structures, which resemble lymph nodes, are associated with effective suppression of TB, and that granulomas that don't contain them are associated with active TB. They also learned that immune cells called T cells that had a surface marker molecule called CXCR5 were associated with the presence of ectopic lymphoid structures.

It's akin to reporting a break-in, Dr. Khader said. If a person calls 911 because of a robbery, but doesn't give a specific address, the immune system police could come to the neighborhood but don't know for certain which home was invaded.

"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," she explained. "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."

When the researchers delivered CXCR5 T cells from donor animals to TB-infected mice that lacked CXCR5, T cell localization and ectopic lymphoid structure formation was restored, leading to decreased susceptibility to TB.

"The protective power of CXCR5 points us in a novel direction for future management of TB," Dr. Khader said. "These findings have powerful implications for the development of vaccines to prevent infection."




The above story is based on materials provided by University of Pittsburgh Schools of the Health Sciences.

Translate this page: Chinese French German Italian Japanese Korean Portuguese Russian Spanish


comments powered by Disqus


Related »

Infection 
5/24/10 
Mount Sinai Discovers Bone Marrow Plays Critical Role in Enhancing Immune Response to Viruses
Researchers at Mount Sinai School of Medicine for the first time have determined that bone marrow cells play a …
Lung 
10/4/11 

Rebooting the System: Immune Cells Repair Damaged Lung Tissues After Flu Infection
Infection 
5/21/12 
T Cell Imbalance Increases Risk for Gastrointestinal Infection Recurrence
CINCINNATI—University of Cincinnati (UC) researchers have found that an imbalance in the regulation of certain T cells—the cells in …
Cells 
8/29/14 
The Early Cost of HIV
Researchers at UC Davis have made some surprising discoveries about the body's initial responses to HIV infection. Studying simian …
Infection 
11/29/12 
Molecular Root of 'Exhausted' T Cells in Chronic Viral Infection
PHILADELPHIA - When you get an acute infection, such as influenza, the body generally responds with a coordinated response …
Cmv 
4/21/10 
Fetuses Can Fight Cytomegalovirus (CMV) Infection: A Novel Unconventional Immune Response Discovered at the Institute for Medical Immunology
The fetus and infant are highly susceptible to viral infections. A number of viruses, including human cytomegalovirus (CMV), cause …
Cells 
9/22/10 
Discovery May Pave Way for New Approaches to Prevent Infections in the Womb
Researchers funded by the Biotechnology and Biological Sciences Research Council (BBSRC) have established in mice the mechanism that detects …
Viral 
7/1/13 
Placental Cells May Prevent Viruses from Passing from Mother to Baby, Says Pitt/MWRI Team
PITTSBURGH, July 1, 2013 – Cells of the placenta may have a unique ability to prevent viruses from crossing …
Ebola 
5/3/11 
Research Team Identifies Receptor for Ebola Virus
A team of researchers has identified a cellular protein that acts as a receptor for Ebola virus and Marburg …
Flu 
8/18/14 
Club Cells Are 'Bad Guys' During Flu Infection
A specialized subset of lung cells can shake flu infection, yet they remain stamped with an inflammatory gene signature …
Cells 
4/8/14 
UNC Researchers Find Genetic Trigger for RSV-induced Infant Hospitalizations
April 8, 2014 CHAPEL HILL, N.C. – Researchers at UNC School of Medicine have pinpointed a viral protein that …
More » 
 
© Newsline Foundation  |  About  |  Privacy Policy  |  Feedback  |  Mobile