What is it about?
This manuscript describes the molecular mechanism of the interferon gamma induced autophagy. Interferon gamma induced autophagy plays a critical role in clearance of several pathogens including Mycobacterium, the causative agent of Tuberculosis. This study demonstrates that exposure of macrophages to interferon gamma leads to increased intracellular calcium levels in a heme oxygenase-1 dependent manner. Heme oxygenase is a stress responsive and cytoprotective enzyme. The increased calcium levels then induces the phosphatase calcineurin to dephosphorylate transcription factor EB (TFEB). TFEB is a master regulator of autophagy. The phosphorylated form of TFEB localizes in the cytoplasm, while the dephosphorylated form resides in the nucleus. Once inside the nucleus, TFEB induces transcription of genes encoding for lysosomal biogenesis and autophagy. In this manner, interferon gamma induced autophagy in macrophage cells to eliminate the pathogens such as Mycobacterium tuberculosis.
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Why is it important?
This study is important as it unravels the signalling cascade the govern the induction of autophagy by interferon gamma.
Perspectives
Activation of macrophages by Interferon gamma induces cellular pathways that help them to eliminate intracellular pathogens. One of such pathways is autophagy. This study explores the mechanism of activation of autophagy in response to interferon gamma. We believe that the pathway described in this study is the primary pathway for mediating autophagy in response to interferon gamma.
Ashwani Kumar
CSIR-Institute of Microbial Technology, Chandigarh, India
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This page is a summary of: Antimycobacterial effect of IFNG (interferon gamma)-induced autophagy is dependent on the HMOX1 (heme oxygenase 1)-mediated increase in the intracellular calcium levels and modulation of PPP3/calcineurin-TFEB (transcription factor EB) axis, Autophagy, February 2018, Taylor & Francis,
DOI: 10.1080/15548627.2018.1436936.
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