Research Topics
Genomes and Genes | Buka SamtenSummaryAffiliation: University of Texas Health Center Country: USA Publications
| Collaborators
|
Detail Information
Publications
Immune regulatory activities of early secreted antigenic target of 6-kD protein of Mycobacterium tuberculosis and implications for tuberculosis vaccine designBuka Samten
Center for Pulmonary and Infectious Disease Control, The University of Texas Health Science Center, Tyler, TX 75708, USA
Tuberculosis (Edinb) 91:S114-8. 2011..Understanding the molecular mechanisms through which ESAT-6 inhibits immunity will permit design of ESAT-6-based vaccine constructs that elicit protective immune responses with minimal negative effects...- An antibody against the surfactant protein A (SP-A)-binding domain of the SP-A receptor inhibits T cell-mediated immune responses to Mycobacterium tuberculosisBuka Samten
Department of Microbiology and Immunology, the Center for Pulmonary and Infectious Disease Control, The University of Texas Health Center, 11937 U S Hwy 271, Tyler, TX 75708, USA
J Leukoc Biol 84:115-23. 2008..Together, these findings support the hypothesis that SP-A, via SP-R210, suppresses cell-mediated immunity against M. tuberculosis via a mechanism that up-regulates secretion of IL-10 and TGF-beta1... 
Mycobacterium tuberculosis ESX-1 system-secreted protein ESAT-6 but not CFP10 inhibits human T-cell immune responsesBuka Samten
Center for Pulmonary and Infectious Disease Control, University of Texas Health Science Center, Tyler, TX 75708 3154, USA
Tuberculosis (Edinb) 89:S74-6. 2009..We conclude that ESAT-6 directly inhibits human T-cell responses by affecting TCR signaling pathways downstream of ZAP70...- CREB, ATF, and AP-1 transcription factors regulate IFN-gamma secretion by human T cells in response to mycobacterial antigenBuka Samten
Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, Tyler, TX 75708, USA
J Immunol 181:2056-64. 2008..Additionally, ATF-2 controls expression of CREB and c-Jun during T cell activation... 
Cyclic AMP response element-binding protein positively regulates production of IFN-gamma by T cells in response to a microbial pathogenBuka Samten
Center for Pulmonary and Infectious Disease Control, Department of Microbiology and Immunology, University of Texas Health Center, Tyler, TX 75708, USA
J Immunol 174:6357-63. 2005..These findings demonstrate that CREB positively regulates IFN-gamma production by human T cells that respond to M. tuberculosis...- NK cells regulate CD8+ T cell effector function in response to an intracellular pathogenRamakrishna Vankayalapati
Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, 11937 US Highway 271, Tyler, TX 75708, USA
J Immunol 172:130-7. 2004..tuberculosis and other intracellular pathogens... - IS6110 functions as a mobile, monocyte-activated promoter in Mycobacterium tuberculosisHassan Safi
Department of Microbiology, Center for Pulmonary and Infectious Disease Control, University of Texas Health Center at Tyler, 11937 US Highway 271, Tyler, TX 75708-3154, USA
Mol Microbiol 52:999-1012. 2004..The ability to activate genes during infection suggests that IS6110 has the potential to influence growth characteristics of different strains, and indicates another mechanism by which IS6110 can impact M. tuberculosis evolution... - Vaccination strategies to enhance local immunity and protection against Mycobacteriun tuberculosisPeter Klucar
Center for Pulmonary and Infectious Disease Control, University of Texas Health Science Center at Tyler, Tyler, TX 75708, United States
Vaccine 27:1816-24. 2009..We conclude that CFP10 is a potential vaccine candidate and that coating vaccines with PEI enhances local protective immunity to tuberculosis.. - Activation of the eis gene in a W-Beijing strain of Mycobacterium tuberculosis correlates with increased SigA levels and enhanced intracellular growthShiping Wu
Department of Microbiology and Immunology, University of Texas Health Science Center at Tyler, Tyler, TX 75708 3154, USA
Microbiology 155:1272-81. 2009..tuberculosis strain 210 to grow in monocytes... - ESAT-6 inhibits production of IFN-gamma by Mycobacterium tuberculosis-responsive human T cellsXisheng Wang
Department of Microbiologyand Immunology, Center for Pulmonary and Infectious Disease Control, University of Texas Health Science Center, Tyler, TX 75708, USA
J Immunol 182:3668-77. 2009..We conclude that ESAT-6 directly inhibits human T cell responses to mycobacterial Ags by affecting TCR signaling pathways downstream of ZAP70... - The principal sigma factor sigA mediates enhanced growth of Mycobacterium tuberculosis in vivoShiping Wu
Department of Microbiology and Immunology, Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, 11937 US Highway 271, Tyler, TX, USA
Mol Microbiol 51:1551-62. 2004..This effect may be mediated in part by increased resistance to reactive oxygen intermediates... - Serum cytokine concentrations do not parallel Mycobacterium tuberculosis-induced cytokine production in patients with tuberculosisRamakrishna Vankayalapati
Center for Pulmonary and Infectious Disease Control, and Department of Microbiology and Immunology, University of Texas Health Center, Tyler, TX 75708-3154, USA
Clin Infect Dis 36:24-8. 2003..tuberculosis-induced cytokine levels, and increased IL-10 serum levels in patients with tuberculosis inhibit IFN-gamma production in response to mycobacterial antigens... - Reduced expression of nuclear cyclic adenosine 5'-monophosphate response element-binding proteins and IFN-gamma promoter function in disease due to an intracellular pathogenBuka Samten
Department of Microbiology and Immunology, and Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, Tyler, TX 75708, USA
J Immunol 168:3520-6. 2002..These data suggest that reduced expression of CREB nuclear proteins in tuberculosis patients results in decreased IFN-gamma promoter activity and reduced IFN-gamma production... - CD40 ligand trimer enhances the response of CD8+ T cells to Mycobacterium tuberculosisBuka Samten
Department of Microbiology and Immunology and Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, Tyler, TX 75708, USA
J Immunol 170:3180-6. 2003..We conclude that CD40LT can enhance CD8(+) T cell effector function in response to M. tuberculosis... - The CD14 receptor does not mediate entry of Mycobacterium tuberculosis into human mononuclear phagocytesHomayoun Shams
Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, 11937 U.S. Highway 271, Tyler, TX 75708-3154, USA
FEMS Immunol Med Microbiol 36:63-9. 2003..tuberculosis; (2) M. tuberculosis infection upregulates CD14 expression on mononuclear phagocytes, and this may facilitate the pathogen's capacity to modulate the immune response... - Exposure to cigarette smoke inhibits the pulmonary T-cell response to influenza virus and Mycobacterium tuberculosisYan Feng
Center for Pulmonary and Infectious Disease Control, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA
Infect Immun 79:229-37. 2011..tuberculosis and influenza virus in a physiologically relevant animal model, increasing susceptibility to both pathogens... - The Mycobacterium tuberculosis early secreted antigenic target of 6 kDa inhibits T cell interferon-γ production through the p38 mitogen-activated protein kinase pathwayHui Peng
Center for Pulmonary and Infectious Disease Control, University of Texas Health Science Center, Tyler, Texas 75708, USA
J Biol Chem 286:24508-18. 2011..Silencing of p38α MAPK with siRNA rendered T cells resistant to ESAT-6 inhibition of IFN-γ production. Taken together, our results demonstrate that ESAT-6 inhibits T cell IFN-γ production in a p38 MAPK-dependent manner... - Multiple Chlamydia pneumoniae antigens prime CD8+ Tc1 responses that inhibit intracellular growth of this vacuolar pathogenBenjamin Wizel
Center for Pulmonary and Infectious Disease Control, Department of Microbiology and Immunology, University of Texas Health Center, Tyler 75708, USA
J Immunol 169:2524-35. 2002.... - Evidence for complex interactions of stress-associated regulons in an mprAB deletion mutant of Mycobacterium tuberculosisXiuhua Pang
Department of Microbiology and Immunology, Center for Pulmonary and Infectious Disease Control, University of Texas Health Center at Tyler, 11937 US Highway 271, Tyler, TX 75708 3154, USA
Microbiology 153:1229-42. 2007.... - Characterization of effector functions of human peptide-specific CD4+ T-cell clones for an intracellular pathogenPeter Klucar
Department of Microbiology and Immunology, University of Texas Health Center at Tyler, Tyler, TX, USA
Hum Immunol 69:475-83. 2008.... - Progress in understanding the human immune responses to Mycobacterium tuberculosisPeter F Barnes
Department of Medicine, The University of Texas Health Science Center at Tyler, Tyler, TX, USA
Tuberculosis (Edinb) 89:S5-9. 2009.... - Early secreted antigenic target of 6-kDa protein of Mycobacterium tuberculosis primes dendritic cells to stimulate Th17 and inhibit Th1 immune responsesXisheng Wang
Center for Pulmonary and Infectious Disease Control, University of Texas Health Science Center, Tyler, TX 75708, USA
J Immunol 189:3092-103. 2012..We conclude that ESAT-6 increases DC production of IL-23 and IL-1β while inhibiting that of IL-12, thus enhancing Th17 at the expense of protective Th1 responses... - Priming reverse transcription with oligo(dT) does not yield representative samples of Mycobacterium tuberculosis cDNADavid L Lakey
Center for Pulmonary and Infectious Disease Control, and Department of Microbiology, University of Texas Health Center, Tyler, TX 75708, USA
Microbiology 148:2567-72. 2002..tuberculosis microarray. These data demonstrate that priming of reverse transcription of mycobacterial mRNA with oligo(dT) does not yield representative samples of cDNA... - The NKp46 receptor contributes to NK cell lysis of mononuclear phagocytes infected with an intracellular bacteriumRamakrishna Vankayalapati
Center for Pulmonary and Infectious Disease Control, University of Texas Health Center, Tyler, TX 75708, USA
J Immunol 168:3451-7. 2002.... - Tyrosine phosphatase PTP-MEG2 negatively regulates vascular endothelial growth factor receptor signaling and function in endothelial cellsQin Hao
Department of Biochemistry, University of Texas Health Science Center, Tyler, Texas 75708, USA
Am J Physiol Cell Physiol 303:C548-53. 2012..Thus we have indentified VEGFR2 as a PTP-MEG2 substrate, and our findings indicate that PTP-MEG2 is a negative regulator of VEGFR2 signaling and function in ECs...