Genetic determination of the effect of post-translational modification on the innate immune response to the 19 kDa lipoprotein of Mycobacterium tuberculosis

[1]  M. Madan Babu,et al.  A Database of Bacterial Lipoproteins (DOLOP) with Functional Assignments to Predicted Lipoproteins , 2006, Journal of bacteriology.

[2]  I. Orme,et al.  Virulent clinical isolates of Mycobacterium tuberculosis grow rapidly and induce cellular necrosis but minimal apoptosis in murine macrophages , 2006, Journal of leukocyte biology.

[3]  H. S. Warren,et al.  Toll-like receptors. , 2005, Critical care medicine.

[4]  J. Wain,et al.  Effect of Deletion or Overexpression of the 19-Kilodalton Lipoprotein Rv3763 on the Innate Response to Mycobacterium tuberculosis , 2005, Infection and Immunity.

[5]  C. Espitia,et al.  The 19-kDa antigen of Mycobacterium tuberculosis is a major adhesin that binds the mannose receptor of THP-1 monocytic cells and promotes phagocytosis of mycobacteria. , 2005, Microbial pathogenesis.

[6]  C. Locht,et al.  Mycobacterium tuberculosis with Disruption in Genes Encoding the Phosphate Binding Proteins PstS1 and PstS2 Is Deficient in Phosphate Uptake and Demonstrates Reduced In Vivo Virulence , 2005, Infection and Immunity.

[7]  R. Wilkinson,et al.  The stress‐responsive chaperone α‐crystallin 2 is required for pathogenesis of Mycobacterium tuberculosis , 2004, Molecular microbiology.

[8]  D. Galati,et al.  Induction of apoptosis and release of interleukin-1 beta by cell wall-associated 19-kDa lipoprotein during the course of mycobacterial infection. , 2004, The Journal of infectious diseases.

[9]  D. Golenbock,et al.  Innate Immune Responses to Rhodococcus equi4 , 2004, The Journal of Immunology.

[10]  S. Ehlers,et al.  Lipoprotein processing is required for virulence of Mycobacterium tuberculosis † , 2004, Molecular microbiology.

[11]  S. Fortune,et al.  Mycobacterium tuberculosis Inhibits Macrophage Responses to IFN-γ through Myeloid Differentiation Factor 88-Dependent and -Independent Mechanisms1 , 2004, The Journal of Immunology.

[12]  Richard J. Laws,et al.  A Common Dominant TLR5 Stop Codon Polymorphism Abolishes Flagellin Signaling and Is Associated with Susceptibility to Legionnaires' Disease , 2003, The Journal of experimental medicine.

[13]  C. Harding,et al.  Alternate Class I MHC Antigen Processing Is Inhibited by Toll-Like Receptor Signaling Pathogen-Associated Molecular Patterns: Mycobacterium tuberculosis 19-kDa Lipoprotein, CpG DNA, and Lipopolysaccharide1 , 2003, The Journal of Immunology.

[14]  C. Harding,et al.  Inhibition of IFN-γ-Induced Class II Transactivator Expression by a 19-kDa Lipoprotein from Mycobacterium tuberculosis: A Potential Mechanism for Immune Evasion1 , 2003, The Journal of Immunology.

[15]  N. Reiner,et al.  The 19-kDa Mycobacterium tuberculosis Protein Induces Macrophage Apoptosis Through Toll-Like Receptor-21 , 2003, The Journal of Immunology.

[16]  Siamon Gordon,et al.  Pattern Recognition Receptors Doubling Up for the Innate Immune Response , 2002, Cell.

[17]  T. Seya,et al.  A lipoprotein family from Mycoplasma fermentans confers host immune activation through Toll-like receptor 2. , 2002, The international journal of biochemistry & cell biology.

[18]  E. Fikrig,et al.  Hyporesponsiveness to vaccination with Borrelia burgdorferi OspA in humans and in TLR1- and TLR2-deficient mice , 2002, Nature Medicine.

[19]  D. Golenbock,et al.  Toll-Like Receptor 2-Dependent Inhibition of Macrophage Class II MHC Expression and Antigen Processing by 19-kDa Lipoprotein of Mycobacterium tuberculosis1 , 2001, The Journal of Immunology.

[20]  G. Kaplan,et al.  Mycobacterium tuberculosis 19-Kilodalton Lipoprotein Inhibits Mycobacterium smegmatis-Induced Cytokine Production by Human Macrophages In Vitro , 2001, Infection and Immunity.

[21]  S. Akira,et al.  [Induction of direct antimicrobial activity through mammalian toll-like receptors]. , 2001, Pneumologie.

[22]  M. Prevost,et al.  Lipoprotein Access to MHC Class I Presentation During Infection of Murine Macrophages with Live Mycobacteria1 , 2001, The Journal of Immunology.

[23]  A. Aderem,et al.  The repertoire for pattern recognition of pathogens by the innate immune system is defined by cooperation between toll-like receptors. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[24]  A. Gallagher,et al.  Analysis of post‐translational modification of mycobacterial proteins using a cassette expression system , 2000, FEBS letters.

[25]  J. Keane,et al.  Macrophage apoptosis in mycobacterial infections , 1999, Journal of leukocyte biology.

[26]  B. Bloom,et al.  Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors. , 1999, Science.

[27]  P. Ricciardi-Castagnoli,et al.  Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene. , 1998, Science.

[28]  J. Keane,et al.  Pathogenic Mycobacterium tuberculosis evades apoptosis of host macrophages by release of TNF-R2, resulting in inactivation of TNF-alpha. , 1998, Journal of immunology.

[29]  J. Herrmann,et al.  Bacterial glycoproteins: a link between glycosylation and proteolytic cleavage of a 19 kDa antigen from Mycobacterium tuberculosis. , 1996, The EMBO journal.

[30]  W. Jacobs,et al.  Site-specific integration of mycobacteriophage L5: integration-proficient vectors for Mycobacterium smegmatis, Mycobacterium tuberculosis, and bacille Calmette-Guérin. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[31]  E. Myers,et al.  Basic local alignment search tool. , 1990, Journal of molecular biology.

[32]  J. Belisle,et al.  N-Terminal clustering of the O-glycosylation sites in the Mycobacterium tuberculosis lipoprotein SodC. , 2009, Glycobiology.

[33]  S. Kaufmann,et al.  Apoptotic vesicles crossprime CD8 T cells and protect against tuberculosis. , 2006, Immunity.

[34]  D. Young,et al.  Lipoprotein antigens ofMycobacterium tuberculosis , 1991 .