Mycobacterium tuberculosis subverts the TLR-2-MyD88 pathway to facilitate its translocation into the cytosol

Mycobacterium tuberculosis (M.tb) has evolved mechanisms to evade its destruction in phagolysosomes, where it successfully survives and replicates within phagocytes. Recent studies have shown that virulent strains of M.tb can translocate from the phagosome into the cytosol of dendritic cells (DC). T...

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Veröffentlicht in:	PloS one 2014-01, Vol.9 (1), p.e86886
Hauptverfasser:	Rahman, Aejazur, Sobia, Parveen, Gupta, Neeta, Kaer, Luc Van, Das, Gobardhan
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antigens Bacillus Calmette-Guerin vaccine Bacterial Translocation - physiology BCG Biology Biotechnology Confining Cytosol Cytosol - metabolism Dendritic cells Digitonin DNA Primers - genetics ESAT-6 antigen Genetic engineering Glycerol Immunology Infections Laboratories Loci Lymphocytes Macrophages Macrophages, Peritoneal Medicine Mice Mice, Inbred C57BL Microscopy, Confocal Molecular modelling Mutants Mycobacterium bovis Mycobacterium tuberculosis Mycobacterium tuberculosis - metabolism Mycobacterium tuberculosis - pathogenicity Mycobacterium tuberculosis - physiology MyD88 protein Myeloid Differentiation Factor 88 - metabolism Phagocytes Phagolysosomes Real-Time Polymerase Chain Reaction Signal transduction Signal Transduction - physiology Signaling Studies Thioglycolates TLR2 protein Toll-Like Receptor 2 - metabolism Toll-like receptors Translocation Tuberculosis Vaccines Virulence (Microbiology)
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