Mycobacterium tuberculosis (Mtb) induces necrotic cell death of infected macrophages, which contributes to tissue necrosis and the progressive loss of lung function during tuberculosis. Mtb can induce multiple forms of programmed necrosis, including necroptosis, pyroptosis and ferroptosis. Concurrently, Mtb also inhibits apoptosis to prevent a host-beneficial cell death response. This paper will first provide an overview of the programmed cell death pathways relevant to Mtb infection. It will then discuss how Mtb activates and manipulates these pathways under different conditions, including a comparison of the findings across mouse, human, and zebrafish-derived macrophages.
Ding et al. (Tue,) studied this question.