IL-1β has been shown to up-regulate miR-146a expression in THP-1 monocytes by activating its NFκB-dependent transcription (31). Meth treatment of CD4+ T-cells increased extracellular IL-1β levels followed by enhanced miR-146a and IL-1β mRNA expression, and decreased TRAF6 protein expression. These results suggested that Meth may modulate the innate immune response via IL-1β signaling to enhance miR-146a and IL-1β mRNA and decrease TRAF6. To address this hypothesis, we blocked IL-1 signaling by employing an IL-1 Receptor Antagonist (IL-1RA).