Daniel L Barber

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Immune reconstitution inflammatory syndrome: the trouble with immunity when you had none
    Daniel L Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rm 6146, 50 South Drive, Bethesda, Maryland, 20892, USA
    Nat Rev Microbiol 10:150-6. 2012
  2. doi request reprint CD4 T cells promote rather than control tuberculosis in the absence of PD-1-mediated inhibition
    Daniel L Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 186:1598-607. 2011
  3. pmc Th1-driven immune reconstitution disease in Mycobacterium avium-infected mice
    Daniel L Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 50 South Drive, Bethesda, MD 20892, USA
    Blood 116:3485-93. 2010
  4. pmc Redundant and pathogenic roles for IL-22 in mycobacterial, protozoan, and helminth infections
    Mark S Wilson
    Immunopathogensis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 184:4378-90. 2010
  5. pmc Innate and adaptive interferons suppress IL-1α and IL-1β production by distinct pulmonary myeloid subsets during Mycobacterium tuberculosis infection
    Katrin D Mayer-Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 35:1023-34. 2011
  6. pmc Cord factor and peptidoglycan recapitulate the Th17-promoting adjuvant activity of mycobacteria through mincle/CARD9 signaling and the inflammasome
    Kevin Shenderov
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute for Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 190:5722-30. 2013
  7. pmc Caspase-1 independent IL-1beta production is critical for host resistance to mycobacterium tuberculosis and does not require TLR signaling in vivo
    Katrin D Mayer-Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 184:3326-30. 2010
  8. pmc Elevated frequencies of highly activated CD4+ T cells in HIV+ patients developing immune reconstitution inflammatory syndrome
    Lis R V Antonelli
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
    Blood 116:3818-27. 2010
  9. pmc Plasma heme oxygenase-1 levels distinguish latent or successfully treated human tuberculosis from active disease
    Bruno B Andrade
    Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 8:e62618. 2013
  10. doi request reprint Role of IL-6 in Mycobacterium avium-Associated Immune Reconstitution Inflammatory Syndrome
    Daniel L Barber
    T Lymphocyte Biology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
    J Immunol 192:676-82. 2014

Collaborators

Detail Information

Publications11

  1. pmc Immune reconstitution inflammatory syndrome: the trouble with immunity when you had none
    Daniel L Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rm 6146, 50 South Drive, Bethesda, Maryland, 20892, USA
    Nat Rev Microbiol 10:150-6. 2012
    ....
  2. doi request reprint CD4 T cells promote rather than control tuberculosis in the absence of PD-1-mediated inhibition
    Daniel L Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 186:1598-607. 2011
    ..Thus, in the absence of the PD-1 pathway, M. tuberculosis benefits from CD4 T cell responses, and host resistance requires inhibition by PD-1 to prevent T cell-driven exacerbation of the infection...
  3. pmc Th1-driven immune reconstitution disease in Mycobacterium avium-infected mice
    Daniel L Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 50 South Drive, Bethesda, MD 20892, USA
    Blood 116:3485-93. 2010
    ..Instead, our findings suggest that mycobacterial-associated IRIS results from a heightened sensitivity of infected lymphopenic hosts to the detrimental effects of Ag-driven CD4 T-cell responses...
  4. pmc Redundant and pathogenic roles for IL-22 in mycobacterial, protozoan, and helminth infections
    Mark S Wilson
    Immunopathogensis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 184:4378-90. 2010
    ..The IL-22 pathway has emerged as a possible target for control of inflammation in certain autoimmune diseases. Our findings suggest that few if any infectious complications would be expected with the suppression of IL-22 signaling...
  5. pmc Innate and adaptive interferons suppress IL-1α and IL-1β production by distinct pulmonary myeloid subsets during Mycobacterium tuberculosis infection
    Katrin D Mayer-Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Immunity 35:1023-34. 2011
    ....
  6. pmc Cord factor and peptidoglycan recapitulate the Th17-promoting adjuvant activity of mycobacteria through mincle/CARD9 signaling and the inflammasome
    Kevin Shenderov
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute for Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 190:5722-30. 2013
    ..Taken together, these findings suggest a general strategy for the rational design of Th17-skewing adjuvants by combining agonists of the CARD9 pathway with inflammasome activators...
  7. pmc Caspase-1 independent IL-1beta production is critical for host resistance to mycobacterium tuberculosis and does not require TLR signaling in vivo
    Katrin D Mayer-Barber
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 184:3326-30. 2010
    ..Together our findings reveal a major role for IL-1beta in host resistance to M. tuberculosis and indicate that during this infection the cytokine can be generated by a mechanism that does not require TLR signaling or caspase-1...
  8. pmc Elevated frequencies of highly activated CD4+ T cells in HIV+ patients developing immune reconstitution inflammatory syndrome
    Lis R V Antonelli
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA
    Blood 116:3818-27. 2010
    ..These studies are registered online at http://clinicaltrials.gov as NCT00557570 and NCT00286767...
  9. pmc Plasma heme oxygenase-1 levels distinguish latent or successfully treated human tuberculosis from active disease
    Bruno B Andrade
    Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 8:e62618. 2013
    ..In addition, we assess correlations between plasma levels of HO-1 and cytokines closely associated with the immunopathogenesis of TB...
  10. doi request reprint Role of IL-6 in Mycobacterium avium-Associated Immune Reconstitution Inflammatory Syndrome
    Daniel L Barber
    T Lymphocyte Biology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
    J Immunol 192:676-82. 2014
    ....
  11. ncbi request reprint Adaptive tolerance and clonal anergy are distinct biochemical states
    Lynda Chiodetti
    Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892, USA
    J Immunol 176:2279-91. 2006
    ..These results demonstrate that T cell adaptive tolerance and clonal anergy are distinct biochemical states, possibly providing T cells with two molecular mechanisms to curtail responsiveness in different biological circumstances...