Andre Bafica

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi The IFN-inducible GTPase LRG47 (Irgm1) negatively regulates TLR4-triggered proinflammatory cytokine production and prevents endotoxemia
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 179:5514-22. 2007
  2. ncbi 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
  3. ncbi 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
  4. ncbi 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
  5. 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
  6. ncbi Cutting edge: TLR9 and TLR2 signaling together account for MyD88-dependent control of parasitemia in Trypanosoma cruzi infection
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 177:3515-9. 2006
  7. pmc The immunity-related GTPase Irgm1 promotes the expansion of activated CD4+ T cell populations by preventing interferon-gamma-induced cell death
    Carl G Feng
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Immunol 9:1279-87. 2008
  8. pmc Intranasal Poly-IC treatment exacerbates tuberculosis in mice through the pulmonary recruitment of a pathogen-permissive monocyte/macrophage population
    Lis R V Antonelli
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA
    J Clin Invest 120:1674-82. 2010
  9. 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
  10. 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

Detail Information

Publications21

  1. ncbi The IFN-inducible GTPase LRG47 (Irgm1) negatively regulates TLR4-triggered proinflammatory cytokine production and prevents endotoxemia
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 179:5514-22. 2007
    ..Thus, our findings reveal a new host-protective function for this GTPase in the response to pathogenic encounter...
  2. ncbi 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...
  3. ncbi 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
    ....
  4. ncbi 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...
  5. 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...
  6. ncbi Cutting edge: TLR9 and TLR2 signaling together account for MyD88-dependent control of parasitemia in Trypanosoma cruzi infection
    Andre Bafica
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 177:3515-9. 2006
    ..Our results reveal that TLR2 and TLR9 cooperate in the control of parasite replication and that TLR9 has a primary role in the MyD88-dependent induction of IL-12/IFN-gamma synthesis during infection with T. cruzi...
  7. pmc The immunity-related GTPase Irgm1 promotes the expansion of activated CD4+ T cell populations by preventing interferon-gamma-induced cell death
    Carl G Feng
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
    Nat Immunol 9:1279-87. 2008
    ..Our studies identify a feedback mechanism in the T helper type 1 response that limits the detrimental effects of IFN-gamma on effector T lymphocyte survival while promoting the antimicrobial functions of IFN-gamma...
  8. pmc Intranasal Poly-IC treatment exacerbates tuberculosis in mice through the pulmonary recruitment of a pathogen-permissive monocyte/macrophage population
    Lis R V Antonelli
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA
    J Clin Invest 120:1674-82. 2010
    ..tuberculosis infection, by promoting the accumulation of a permissive myeloid population in the lung. In addition, these data suggest that agents that stimulate type I IFN should be used with caution in patients exposed to this pathogen...
  9. 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...
  10. 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...
  11. ncbi 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...
  12. ncbi Dectin-1 interaction with Mycobacterium tuberculosis leads to enhanced IL-12p40 production by splenic dendritic cells
    Antonio Gigliotti Rothfuchs
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 179:3463-71. 2007
    ..tuberculosis-induced IL-12p40 production by DC in which the receptor augments bacterial-host cell interaction and enhances the subsequent cytokine response through an unknown mechanism involving Syk signaling...
  13. pmc In situ IL-12/23p40 production during mycobacterial infection is sustained by CD11bhigh dendritic cells localized in tissue sites distinct from those harboring bacilli
    Antonio Gigliotti Rothfuchs
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 182:6915-25. 2009
    ....
  14. pmc Mannose-binding lectin regulates host resistance and pathology during experimental infection with Trypanosoma cruzi
    Antonio Gigliotti Rothfuchs
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA
    PLoS ONE 7:e47835. 2012
    ..These observations point to a previously unappreciated role for MBL in regulating host resistance and cardiac inflammation during infection with a major human pathogen...
  15. ncbi Mice deficient in LRG-47 display enhanced susceptibility to Trypanosoma cruzi infection associated with defective hemopoiesis and intracellular control of parasite growth
    Helton C Santiago
    Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    J Immunol 175:8165-72. 2005
    ..Together, these data establish that LRG-47 can influence pathogen control by simultaneously regulating macrophage-microbicidal activity and hemopoietic function...
  16. pmc TAP-1 indirectly regulates CD4+ T cell priming in Toxoplasma gondii infection by controlling NK cell IFN-gamma production
    Romina S Goldszmid
    Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases NIAID, National Institutes of Health NIH, Bethesda, MD 20892, USA
    J Exp Med 204:2591-602. 2007
    ....
  17. ncbi Anti-inflammatory actions of lipoxin A4 and aspirin-triggered lipoxin are SOCS-2 dependent
    Fabiana S Machado
    Department of Immunology, Duke University Medical Center, Durham, North Carolina 27705, USA
    Nat Med 12:330-4. 2006
    ..We also show that SOCS-2 is a crucial intracellular mediator of the anti-inflammatory actions of aspirin-induced lipoxins in vivo...
  18. ncbi Anti-inflammatory pathways as a host evasion mechanism for pathogens
    Julio Aliberti
    Department of Immunology, Duke University Medical Center, Durham, NC 27705, USA
    Prostaglandins Leukot Essent Fatty Acids 73:283-8. 2005
    ....
  19. ncbi Neisseria gonorrhoeae enhances infection of dendritic cells by HIV type 1
    Jizhong Zhang
    Department of Microbiology and Immunology, Division of Infectious Diseases, Walther Oncology Center, Walther Oncology Institute, Indiana University School of Medicine, Indianapolis, IN 46202, USA
    J Immunol 174:7995-8002. 2005
    ..These results provide one potential mechanism through which GC infection increases HIV replication in patients infected with both GC and HIV...
  20. ncbi Cutting edge: dendritic cells are essential for in vivo IL-12 production and development of resistance against Toxoplasma gondii infection in mice
    Cheng hu Liu
    Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA
    J Immunol 177:31-5. 2006
    ..Taken together, the results presented in this study indicate that DCs constitute the major IL-12-producing cell population in vivo during T. gondii infection...
  21. pmc Leishmania infection impairs beta 1-integrin function and chemokine receptor expression in mononuclear phagocytes
    Nathanael F Pinheiro
    LPBI, Centro de Pesquisas Goncalo Moniz, Fundacao Oswaldo Cruz, Rua Waldemar Falcão no 121, Candeal, Salvador, BA 40296 710, Brazil
    Infect Immun 74:3912-21. 2006
    ..8 to 4.1 times and 1.9 to 2.8 times, respectively). Together, these results suggest that mechanisms regulating integrin function are implicated in the change of macrophage adhesion in leishmaniasis...