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Overall, the finding identified a new bacterial factor Rv0158, which improves the understanding of the immune evasion mechanisms of M. tb, and suggests that Rv0158 may indirectly facilitate STING degradation or modulate its stability through host-interacting partners.
Findings identify a previously uncharacterized mechanism by which M. tb dampens the IFN-I response by targeting TBK1, highlighting Rv3248c as a contributor to pathogenesis and a potential therapeutic target.
A genome-wide CRISPR-KO library is constructed and results indicate that SH3PXD2B is a critical host factor manipulated by M. bovis to promote macrophage phagocytosis and inhibit migration, thereby facilitating bacterial invasion and reveal a new pathogenic strategy.
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