Subversion from the Sidelines

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Science  22 Jan 2010:
Vol. 327, Issue 5964, pp. 417-418
DOI: 10.1126/science.1185569

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Mycobacterium tuberculosis, which kills 1.7 million people annually, is a pathogen that proliferates within macrophages of the immune system. The granuloma—the hallmark lesion of tuberculosis—forms from repeated waves of macrophages that arrive at the site of infection to combat the pathogen, only to be themselves infected by bacteria multiplying within their dying predecessors. A central tenet in the characterization of tuberculosis has been that the granuloma represents a host defense response that contains the infection. But could the beneficiary of granuloma formation be the pathogen itself rather than the host? On page 466 in this issue, Volkman et al. show that a secreted bacterial peptide and secreted host cell protein are key to stimulating early granuloma development and maintaining the infection (1). The simplest interpretation is that the pathway constitutes a deliberate pro-granulomatous virulence mechanism that benefits the bacteria.