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- W2023696968 abstract "Autophagy, an evolutionary highly conserved process in virtually all eukaryotic cells, involves the sequestration of cytosol regions within double-membrane bound compartments and delivery of the contents to the lysosomes for degradation. Rapidly accumulating evidence has shown that autophagy is a component of innate immunity and is involved in host defense elimination of pathogens. Our previous studies show that Toll-like receptor 4 (TLR4) is a sensor for autophagy associated with innate immunity. We, now, further demonstrate that LPS or poly(I:C)-treatment significantly reduced mycobacterial viability in mouse macrophages. In addition, LPS reduction of mycobacterial viability was abrogated with the use of autophagy inhibitor 3-MA and in autophagy deficient macrophages. These findings demonstrate that TLR3 or TLR4 stimulation induces autophagy-mediated elimination of mycobacteria in macrophages. These results provide groundwork for therapeutic strategies directed at elimination of mycobacterial infections in macrophages." @default.
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- W2023696968 date "2013-12-01" @default.
- W2023696968 modified "2023-10-18" @default.
- W2023696968 title "Harnessing of TLR-mediated autophagy to combat mycobacteria in macrophages" @default.
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- W2023696968 doi "https://doi.org/10.1016/s1472-9792(13)70008-8" @default.
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