Using a TLR4-activating virulent strain of M. tuberculosis that induces high levels of type I IFN, we detected increased levels of arginase 1 (Arg1) gene expression in the lungs, along with other genes associated with alternatively activated macrophages, when IFNAR signaling was abrogated in IFN-γR–deficient mice following in vivo infection. This evidence concerns the gene TLR4 and infection.