The TLR2 gene promoter contains multiple binding sites for transcriptional factors, which include NF-κB, CCAAT/enhancer binding protein, cAMP response element-binding protein and STAT (signal transducer and activator of transcription) (117) . Of these, NF-κB has been reported to regulate TLR2 expression in response to cytokines and mycobacterial infection (117, 118) . It has been demonstrated that LPS-TLR4-induced TLR2 upregulation in AMφ is largely mediated through the NF-κB signaling pathway, because the NF-κB inhibitor IKK-NBD significantly decreased LPS-induced TLR2 expression in AMφ (115) . Although oxidants are involved in the NF-κB signal transduction pathway (119) (120) (121) , their molecular targets have not yet been defined. The contribution of redox regulation and location of potential redox-sensitive sites within the NF-κB activation pathway are the subjects of controversy (119) .