Samten, Buka, M.D., M.S.

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Contact: buka.samten@uthct.edu

Education:
M.D., Xinjiang Medical University, 1987, Urumqi, China
M.S., Immunology, Peking University, School of Medicine, 1996, Beijing, China

Research Interest:
TUBERCULOSIS

Current Projects:
Evaluation of intracellular signaling molecules that control production of interferon-g in peripheral blood lymphocytes in response to M. tuberculosis.

Research Overview:
Understanding the immunopathological mechanisms of human tuberculosis by evaluating the intracellular signaling molecules in human peripheral blood lymphocytes that regulate the production of interferon-g, one of the most important cytokines that confer protection against M. tuberculosis.

Tuberculosis causes two million deaths annually world-wide, and mortality rates are increasing with the spread of HIV and multidrug-resistant tuberculosis. Global control of tuberculosis hinges on development of an effective vaccine, which, in turn, depends on understanding the human immune response to M. tuberculosis infection. T-lymphocytes are the major cells that mediate protection against tuberculosis, and they do so in part by secretion of a soluble factor called interferon-g. Studies from our laboratory and others showed that IFN-g production by peripheral blood lymphocytes from most tuberculosis patients is reduced, compared to the findings in normal donors. Understanding the mechanisms of reduced production of IFN-g will help us to understand why some people are more susceptible to tuberculosis, and allow development of new strategies to reduce this susceptibility and provide protection against the disease.

Selected Papers and Abstracts:

• Samten B, Howard ST, Weis SE, Wu S, Shams H, Townsend JC, Safi H, Barnes PF. Cyclic AMP response element-binding protein positively regulates production of IFN-gamma by T cells in response to a microbial pathogen. Journal of Immunology, 174: 6357–6363, 2005.
• Safi H, Barnes PF, Lakey DL, Shams H, Samten B, Vankayalapati R, Howard ST. IS6110 functions as a mobile, monocyte-activated promoter in Mycobacterium tuberculosis. Molecular Microbiology. 52: 999-1012, 2004.
• Wu S, Howard ST, Lakey DL, Kipnis A, Samten B, Safi H, Gruppo V, Wizel B, Shams H, Basaraba RJ, Orme IM, Barnes PF. The principal sigma factor sigA mediates enhanced growth of Mycobacterium tuberculosis in vivo. Molecular Microbiology, 51: 1551-1562, 2004.
• Samten B, Wizel B, Shams H, Weis SE, Klucar P, Wu S, Vankayalapati R, Thomas EK, Okada S, Krensky AM, Barnes PF. CD40 ligand trimer enhances the response of CD8+ T cells to Mycobacterium tuberculosis. J Immunology. 170(6):3180-6, 2003.
• Wizel B, Starcher BC, Samten B, Chroneos Z, Barnes PF, Dzuris J, Higashimoto Y, Appella E, Sette A. Multiple Chlamydia pneumoniae antigens prime CD8+ Tc1 responses that inhibit intracellular growth of this vacuolar pathogen. Journal of Immunology. 169(5):2524-35, 2002.
• Lakey DL, Zhang Y, Talaat AM, Samten B, DesJardin LE, Eisenach KD, Johnston SA, Barnes PF. Priming reverse transcription with oligo(dT) does not yield representative samples of Mycobacterium tuberculosis cDNA. Microbiology. 148(Pt 8):2567-72, 2002.
• Samten B, Ghosh P, Yi AK, Weis SE, Lakey DL, Gonsky R, Pendurthi U, Wizel B, Zhang Y, Zhang M, Gong J, Fernandez M, Safi H, Vankayalapati R, Young HA, Barnes PF. Reduced expression of nuclear cyclic adenosine 5’-monophosphate response element-binding proteins and IFN-gamma promoter function in disease due to an intracellular pathogen. Journal of Immunology. 168(7):3520-6, 2002.
• Shams H, Wizel B, Weis SE, Samten B, Barnes PF. Contribution of CD8(+) T cells to gamma interferon production in human tuberculosis. Infection & Immunity. 69(5):3497-501, 2001.
• Vankayalapati R, Wizel B, Weis SE, Samten B, Girard WM, Barnes PF. Production of interleukin-18 in human tuberculosis. Journal of Infectious Diseases. 182(1):234-9, 2000.