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In that regard, recent work with the AS3MT knockout mouse has been extremely revealing in that it clearly demonstrates the importance of arsenic methylation in facilitating elimination and decreasing tissue retention (Drobna et al

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In addition, Irg1-deficient phagocytes, which cannot produce itaconate, have shown increased susceptibility to M.tb infection, with infected mice exhibiting higher bacterial loads, reduced survival, exacerbated inflammation, extensive necrotizing granuloma formation and elevated neutrophil infiltration in the lungs [104, 105]