Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), is responsible for nearly 2 million deaths each year. The rise in HIV co-infections and the neglect of TB control programs has led to TB's re-emergence as a serious public health concern.  An improved understanding of host immune responses following Mycobacterium infection can provide insights into the pathogenesis of virulent mycobacteria and identify potential targets for rational anti-TB drug design. Our work indicates that infection with isogenic strains of M. tuberculosis results in differential activation of various transcription factors. Previous studies have demonstrated that expression of the folate receptor (FR) is primarily restricted to tumor cells and activated macrophages. We hypothesize that the FR may also be expressed on activated, tuberculosis-infected macrophages. Addressing the biology behind FR expression in Mycobacterium-infected mouse and human macrophages may lead to new mechanisms to treat drug-sensitive and drug-resistant tuberculosis.