This mechanism has been shown to be important in the immune system's response to tuberculosis; TLR stimulation of human macrophages up-regulates the expression of VDRs and induces the enzyme (CYP27b1) that catalyzes the conversion of 25(OH)D to 1,25(OH)2D, the biologically active metabolite of vitamin D. In presence of adequate 25(OH)D, VDR upregulation leads to cathelicidin induction, an antimicrobial peptide with direct action against intracellular pathogens including Mycobacterium tuberculosis[4], a leading cause of disease progression and mortality among HIV-infected patients [26]. This evidence concerns the gene VDR and tuberculosis.