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