Notably, another study revealed that B. abortus-induced secretion of IL-12p40 in murine splenic DCs was independent of TLR2 [48], and TLR2 knockout mice were able to control B. abortus infection similar as wild-type animals indicating that pathogen-recognition through TLR2 is not essential for resistance to B. abortus in the murine brucellosis model [49], [50]. This evidence concerns the gene TLR2 and brucellosis.