作者: Richard W. Stokes
DOI: 10.1007/978-94-007-4740-1_16
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摘要: Mycobacterium tuberculosis, the etiological agent of is a major pathogen man with about one-third world’s population being infected. M. tuberculosis resides within macrophages which are members host’s cell-mediated immune response that supposedly protect against bacterial invasion. Obviously has strategies enable it to survive in this hostile environment. Amongst many virulence factors possesses two paralogues ubiquitous stress protein, chaperonin (Cpn) or Hsp60 have been named Cpn60.1 and Cpn60.2. While cpn60.2 an essential gene involved maintenance cell viability through “normal” chaperoning activities, cpn60.1 non-essential appears little no involvement protein folding activities. Both Cpn60.2 varied “moonlighting” functions can act as secreted signaling molecules, modulators host immunity, surface located ligands wall components. How these proteins leave cytosol function extracellularly at still not clear. That they becoming clear although recognition by may instead mediate defence mechanism.