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:
Long term goal of our laboratory is to understand the immunopathological mechanisms of human tuberculosis by evaluating the intracellular signaling molecules in human peripheral blood lymphocytes that regulate the production of interferon-gamma, and the effect of Mycobacterium tuberculosis secreted proteins on human immune responses.

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

Immune regulatory functions of M. tuberculosis secreted proteins.


Lay Summary
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-gamma. Studies from our laboratory and others showed that IFN-gamma 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-gamma 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.
We also study the effect of bacterial products from Mycobacterium tuberculosis, specifically the secreted proteins, on human immune responses. Development of tuberculosis is decided by the consequences of a two way interaction process in our body, interaction of Mycobacterium tuberculosis and our immune cells. Bacterial products may play a role in manipulating our immune system to favor bacterial growth in the body, and development of tuberculosis.

Selected Papers and Abstracts:

• Pasquinelli V, Townsend JC, Jurado JO, Alvarez IB, Quiroga MF, Barnes PF, Samten B, Garcia VE. IFN-gamma production during active tuberculosis is regulated by mechanisms that involve IL-17, SLAM and CREB. J Infect Dis. 2009 Mar 1;199(5):661-5.
• Klucar P, Barnes PF, Kong Y, Howard ST, Pang X, Huang F, Tvinnereim A, Samten B, Shams H. Vaccination strategies to enhance mucosal immunity and protection against mycobacterium tuberculosis. Vaccine, 27:1816-1824, 2009.
• Wang X, Barnes PF, Dobod-Elder KM, Townsend JC, Chung Y, Shams H, Weis SE, Samten B.ESAT-6 inhibits production of interferon-gamma by M. tuberculosis-responsive human T cells. Journal of Immunology, 182:3668-3677, 2009.
• Samten B, Townsend JC, Weis SE, Bhoumick A, Klucar P, Shams H, Barnes PF. CREB, ATF and AP-1 Transcription factors regulate IFN-gamma secretion by human T-cells in response to microbial antigen. Journal of Immunology, 181:2056-2064, 2008.
• Samten B, Townsend JC, Sever-Chroneos Z, Pasquinelli V, Barnes PF, Chroneos ZC. An antibody against the surfactant protein A (SP-A)-binding domain of the SP-A receptor inhibits T cell-mediated immune responses to Mycobacterium tuberculosis. Journal of Leukocyte Biology, 84: 115-123, 2008.
• Pang XP, Vu TF, Byrd S, Ghanny P, Soteropoulos GV, Mukamolova S, Wu B, Samten B, Howard ST.
  Evidence for complex interactions of stress-associated regulons in an mprAB deletion mutant of Mycobacterium tuberculosis. Microbiology, 153(4): 1229 – 1242, 2007.
• Samten B, Howard S T, Weis S E, Wu S, Shams H, Townsend JC, Safi H, Barnes PF. Cyclic AMP response element-binding protein positively regulates production of interferon-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 Maycobacterium tuberculosis. Molecular Microbiology. 52: 999-1012, 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.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.