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An increase in NF-κB to a certain unknown level has been shown to be effective as an anti-inflammatory mediator to assist in the fight against tuberculosis
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NF-κB increases IL-2R production and thus reduces the lymphocytic response towards M. tb, thus a substantial increase in NF-κB has been shown to increase the survival of M. tb
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Triple therapy of INH, RIF, PYZ has been shown to be the most effective combination of anti-tb drugs to increase NF-κB
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The activation of TNFR1 activates IκB kinase which phosphorylates IκB proteins to release free NF-κB
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INH, RIF, PYZ administered individually seem to decrease NF-κB activity
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Decreased NF-κB has been shown to allow increased M. tb survival
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NF-κB remains inactive by being bound to IκB proteins
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IκBα and A20 reduce TNFR1 activity, which, in turn, reduce IκB kinase and subsequently reduce free NF-κB
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