ArticleBMC immunology2025
mTORC2 is crucial for regulating the recombinant Mycobacterium tuberculosis CFP-10 protein-induced phagocytosis in macrophages.
Article in BMC immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025Review
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Authors and funding
11 authors.
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Abstract
Mycobacterium tuberculosis (M. tuberculosis, Mtb) is a pathogenic bacterial species in the family Mycobacteriaceae and the causative agent of most cases of tuberculosis. Macrophages play essential roles in defense against invading pathogens, including M. tuberculosis. The study of M. tuberculosis-associated antigens is one of the hotspots of current research. The secreted proteins of M. tuberculosis, including early secretory antigen target 6 (ESTA6) and culture filtrate protein 10 (CFP-10), are crucial for the immunological diagnosis of tuberculosis. However, the relationship of CFP-10 alone with macrophages is still not well understood. In the present study, we report that the purified recombinant protein CFP-10 (rCFP-10) significantly enhanced the phagocytic capacity of murine macrophages. rCFP-10 induces both TNF-α and IL-6 production. Additionally, RNASeq analysis revealed that rCFP10 triggers multiple pathways involved with macrophage activation. Interestingly, neither mitochondrial reactive oxygen species nor lysosomal content had a significant difference treated with rCFP-10 in macrophages. Moreover, inhibition of the mammalian target of rapamycin (mTOR) activity was shown to significantly reverse the rCFP10-induced phagocytosis, various genes involved in lysosome acidification and TLR signaling. These findings highlight that the CFP-10 plays an essential role in the invasion of macrophages by M. tuberculosis, which is partly regulated by the mTORC2 signal pathway.
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