1. ¹Mycobacterial Research Programme, Centenary Institute, Newtown, New South Wales, Australia
2. ²Discipline of Medicine, Central Clinical School, University of Sydney, Sydney, Australia

Correspondence: Dr B Saunders, Mycobacterial Research Programme, Centenary Institute, Locked Bag No 6, Newtown, 2042 New South Wales, Australia. E-mail: b.saunders@centenary.usyd.edu.au

Received 3 November 2006; Revised 7 November 2006; Accepted 8 November 2006; Published online 9 January 2007.

Abstract

During tuberculosis (TB) infection, the granuloma provides the microenvironment in which antigen-specific T cells colocate with and activate infected macrophages to inhibit the growth of Mycobacterium tuberculosis. Although the granuloma is the site for mycobacterial killing, virulent mycobacteria have developed a variety of mechanisms to resist this macrophage-mediated killing. These surviving mycobacteria become dormant, however, if host cellular immunity or the signals maintaining granuloma structure wane, or if mycobacteria resume replication, leading to reactivation of TB. This balance of life and death applies not only to the mycobacterium but also to the host macrophages that may undergo apoptosis or necrosis, leading to the characteristic caseous necrosis within the granuloma, and the potential spread of TB infection. The immunological factors controlling the development and maintenance of the granuloma will be reviewed.