U.S. Pharmacist

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Molecule That Polices TB Infection Found

By staff


1/23/2013
US Pharm. 2013;38(1):HS-18.

According to a study led by researchers at Children’s Hospital of Pittsburgh of UPMC and the University of Pittsburgh (Pitt) School of Medicine, the presence of a certain molecule, called CXCR5, allows the immune system to effectively police tuberculosis (TB) of the lungs and prevent progression into a deadly infection. Their findings appeared on January 3 in the online version of the Journal of Clinical Investigation.

For the NIH-funded study, the researchers studied human TB-infected cells as well animal models. They found that granulomas with ectopic lymphoid structures are associated with effective suppression of TB, and that granulomas that do not contain them are associated with active TB. They also learned that immune cells, called T cells, that had the surface marker CXCR5 molecule were associated with the presence of these protective ectopic lymphoid structures.  

“The protective power of CXCR5 points us in a novel direction for future management of TB,” said senior author Shabaana A. Khader, PhD, assistant professor of pediatrics, Pitt School of Medicine.   “These findings have powerful implications for the development of vaccines to prevent infection.”


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U.S. Pharmacist is a monthly journal dedicated to providing the nation's pharmacists with up-to-date, authoritative, peer-reviewed clinical articles relevant to contemporary pharmacy practice in a variety of settings, including community pharmacy, hospitals, managed care systems, ambulatory care clinics, home care organizations, long-term care facilities, industry and academia. The publication is also useful to pharmacy technicians, students, other health professionals and individuals interested in health management. Pharmacists licensed in the U.S. can earn Continuing Education credits through Postgraduate Healthcare Education, LLC, accredited by the Accreditation Council for Pharmacy Education (ACPE) as a provider of continuing pharmacy education.

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