Charles A Scanga

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Cutting edge: MyD88 is required for resistance to Toxoplasma gondii infection and regulates parasite-induced IL-12 production by dendritic cells
    Charles A Scanga
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 168:5997-6001. 2002
  2. pmc MyD88-deficient mice display a profound loss in resistance to Mycobacterium tuberculosis associated with partially impaired Th1 cytokine and nitric oxide synthase 2 expression
    Charles A Scanga
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Infect Immun 72:2400-4. 2004
  3. ncbi request reprint Mice lacking myeloid differentiation factor 88 display profound defects in host resistance and immune responses to Mycobacterium avium infection not exhibited by Toll-like receptor 2 (TLR2)- and TLR4-deficient animals
    Carl G Feng
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 8003, USA
    J Immunol 171:4758-64. 2003
  4. pmc TLR9 regulates Th1 responses and cooperates with TLR2 in mediating optimal resistance to Mycobacterium tuberculosis
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Exp Med 202:1715-24. 2005
  5. ncbi request reprint Maintenance of pulmonary Th1 effector function in chronic tuberculosis requires persistent IL-12 production
    Carl G Feng
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 8003, USA
    J Immunol 174:4185-92. 2005
  6. ncbi request reprint The induction of Toll-like receptor tolerance enhances rather than suppresses HIV-1 gene expression in transgenic mice
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982, USA
    J Leukoc Biol 75:460-6. 2004
  7. pmc Host control of Mycobacterium tuberculosis is regulated by 5-lipoxygenase-dependent lipoxin production
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA
    J Clin Invest 115:1601-6. 2005
  8. ncbi request reprint Viral gene expression in HIV transgenic mice is activated by Mycobacterium tuberculosis and suppressed after antimycobacterial chemotherapy
    Charles A Scanga
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA
    J Infect Dis 195:246-54. 2007
  9. ncbi request reprint Cutting edge: in vivo induction of integrated HIV-1 expression by mycobacteria is critically dependent on Toll-like receptor 2
    Andre Bafica
    Immunobiology Section, National Institute of Allergy and Infectious Diseases and Chemical Immunology Section, Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 171:1123-7. 2003
  10. pmc TLR2 synergizes with both TLR4 and TLR9 for induction of the MyD88-dependent splenic cytokine and chemokine response to Streptococcus pneumoniae
    Katherine S Lee
    Department of Pathology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA
    Cell Immunol 245:103-10. 2007

Detail Information

Publications12

  1. ncbi request reprint Cutting edge: MyD88 is required for resistance to Toxoplasma gondii infection and regulates parasite-induced IL-12 production by dendritic cells
    Charles A Scanga
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 168:5997-6001. 2002
    ..Taken together, these data suggest that the induction of IL-12 by T. gondii depends on a unique mechanism involving both MyD88 and G protein-coupled signaling pathways...
  2. pmc MyD88-deficient mice display a profound loss in resistance to Mycobacterium tuberculosis associated with partially impaired Th1 cytokine and nitric oxide synthase 2 expression
    Charles A Scanga
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Infect Immun 72:2400-4. 2004
    ..These results argue that resistance to M. tuberculosis must depend on MyD88-dependent signals mediated by an as-yet-undetermined TLR or a combination of TLRs...
  3. ncbi request reprint Mice lacking myeloid differentiation factor 88 display profound defects in host resistance and immune responses to Mycobacterium avium infection not exhibited by Toll-like receptor 2 (TLR2)- and TLR4-deficient animals
    Carl G Feng
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 8003, USA
    J Immunol 171:4758-64. 2003
    ....
  4. pmc TLR9 regulates Th1 responses and cooperates with TLR2 in mediating optimal resistance to Mycobacterium tuberculosis
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Exp Med 202:1715-24. 2005
    ..These findings reveal a previously unappreciated role for TLR9 in the host response to M. tuberculosis and illustrate TLR collaboration in host resistance to a major human pathogen...
  5. ncbi request reprint Maintenance of pulmonary Th1 effector function in chronic tuberculosis requires persistent IL-12 production
    Carl G Feng
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 8003, USA
    J Immunol 174:4185-92. 2005
    ..tuberculosis infection and suggest that breakdown of this mechanism could be a contributing factor in reactivated disease...
  6. ncbi request reprint The induction of Toll-like receptor tolerance enhances rather than suppresses HIV-1 gene expression in transgenic mice
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20982, USA
    J Leukoc Biol 75:460-6. 2004
    ....
  7. pmc Host control of Mycobacterium tuberculosis is regulated by 5-lipoxygenase-dependent lipoxin production
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA
    J Clin Invest 115:1601-6. 2005
    ..tuberculosis...
  8. ncbi request reprint Viral gene expression in HIV transgenic mice is activated by Mycobacterium tuberculosis and suppressed after antimycobacterial chemotherapy
    Charles A Scanga
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA
    J Infect Dis 195:246-54. 2007
    ..tuberculosis on latent HIV expression and for testing therapeutic regimens for reducing the disease burden in patients with acquired immunodeficiency syndrome-associated tuberculosis...
  9. ncbi request reprint Cutting edge: in vivo induction of integrated HIV-1 expression by mycobacteria is critically dependent on Toll-like receptor 2
    Andre Bafica
    Immunobiology Section, National Institute of Allergy and Infectious Diseases and Chemical Immunology Section, Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 171:1123-7. 2003
    ..Together, these results argue that TLR2 plays a crucial role in the activation of HIV-1 expression by mycobacterial coinfections...
  10. pmc TLR2 synergizes with both TLR4 and TLR9 for induction of the MyD88-dependent splenic cytokine and chemokine response to Streptococcus pneumoniae
    Katherine S Lee
    Department of Pathology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA
    Cell Immunol 245:103-10. 2007
    ..These data demonstrate significant synergy between TLR2 and both TLR4 and TLR9 for induction of the MyD88-dependent splenic cytokine and chemokine response to Pn...
  11. ncbi request reprint Influence of coinfecting pathogens on HIV expression: evidence for a role of Toll-like receptors
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 50, Rm 6146, 50 South Drive, Bethesda, MD 20892, USA
    J Immunol 172:7229-34. 2004
    ..Therefore, TLR-pathogen interactions could play an indirect role in regulating HIV-associated disease. In this review, we summarize emerging evidence for the influence of TLR recognition on HIV gene activation and AIDS progression...
  12. ncbi request reprint CD40, but not CD40L, is required for the optimal priming of T cells and control of aerosol M. tuberculosis infection
    Vanja Lazarevic
    Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA
    Immunity 19:823-35. 2003
    ..tuberculosis Hsp70 elicited IL-12 production from WT dendritic cells. This response was absent in both CD40(-/-) dendritic cells and CD40(-/-) mice, suggesting that M. tuberculosis Hsp70 serves as an alternative ligand for CD40 in vivo...