The observed suppression of transcription Ifnb1 post H37Rv-infection may be explained by the production of immunomodulatory lipoproteins signaling through TLR2 or the up-regulation of transcription of Clec4a2, which may inhibit TLR9-induced induction of Ifnb1. Depending on their degree of virulence, different strains of M. tuberculosis induce different levels of pro- and anti-inflammatory responses [45]. This evidence concerns the gene IFNB1 and infection.