Data on tuberculosis detailed by researchers at University of Ulm
2009 JUL 13 - (NewsRx.com) -- "The incidence of tuberculosis is increased during treatment of autoimmune diseases with anti-TNF antibodies. This is a significant clinical complication, but also provides a unique model to study immune mechanisms in human tuberculosis," scientists in Ulm, Germany report. "Given the key role for cell-mediated immunity in host defense against Mycobacterium tuberculosis, we hypothesized that anti-TNF treatment impairs T cell-directed antimicrobial activity. Anti-TNF therapy reduced the expression in lymphocytes of perforin and granulysin, 2 components of the T cell-mediated antimicrobial response to intracellular pathogens. Specifically, M. tuberculosis-reactive CD8(+)CCR7(-)CD45RA(+) effector memory T cells (T-EMRA cells) expressed the highest levels of granulysin, lysed M. tuberculosis, and infected macrophages and mediated an antimicrobial activity against intracellular M. tuberculosis. Furthermore, T-EMRA cells expressed cell surface TNF and bound the anti-TNF therapeutic infliximab in vitro, making them susceptible to complement-mediated lysis. Immune therapy with anti-TNF was associated with reduced numbers of CD8(+) T-EMRA cells and decreased antimicrobial activity against M. tuberculosis, which could be rescued by the addition of CD8(+) T-EMRA cells," wrote H. Bruns and colleagues, University of Ulm. The researchers concluded: "These results suggest that anti-TNF therapy triggers a reduction of CD8(+) T-EMRA cells with antimicrobial activity against M. tuberculosis, providing insight into the mechanism whereby key effector T cell subsets contribute to host defense against tuberculosis.." Bruns and colleagues published their study in the Journal of Clinical Investigation (Anti-TNF immunotherapy reduces CD8(+) T cell-mediated antimicrobial activity against Mycobacterium tuberculosis in humans. Journal of Clinical Investigation, 2009;119(5):1167-1177). For additional information, contact S. Stenger, University of Ulm Medical Center, Institute Med Mikrobiol & Hyg, Albert Einstein Allee 11, D-89081 Ulm, Germany. The publisher's contact information for the Journal of Clinical Investigation is: American Society Clinical Investigation Inc., 35 Research Dr., Ste. 300, Ann Arbor, MI 48103, USA. Keywords: Germany, Ulm, Antimicrobial, Antimicrobials, Autoimmune Diseases, Autoimmune Disorder, Biological Therapy, Cutaneous Tuberculosis, Immunology, Immunotherapy, Mycobacteria, Mycobacterium Tuberculosis, Treatment, University of Ulm. This article was prepared by Tuberculosis Week editors from staff and other reports. Copyright 2009, Tuberculosis Week via NewsRx.com.
|
