Abstract
Tuberculosis (TB) is a major health threat to the human population worldwide. The etiology of the disease is Mycobacterium tuberculosis (Mtb), a highly successful intracellular pathogen. It has the ability to manipulate the host immune response and to make the intracellular environment suitable for its survival. Many studies have addressed the interactions between the bacteria and the host immune cells as involving many immune mediators and other cellular players. Interferon-beta (IFN-beta) signaling is crucial for inducing the host innate immune response and it is an important determinant in the fate of mycobacterial infection. The role of IFN-beta in protection against viral infections is well established and has been studied for decades, but its role in mycobacterial infections remains much more complicated and debatable. The involvement of IFN-beta in immune evasion mechanisms adopted by Mtb has been an important area of investigation in recent years. These advances have widened our understanding of the pro-bacterial role of IFN-beta in host-pathogen interactions. This pro-bacterial activity of IFN-beta appears to be correlated with its anti-inflammatory characteristics, primarily by antagonizing the production and function of interleukin 1 beta (IL-1 beta) and interleukin 18 (IL-18) through increased interleukin 10 (IL-10) production and by inhibiting the nucleotide-binding domain and leucine-rich repeat protein-3 (NLRP3) inflammasome. Furthermore, it also fails to provoke a proper T helper 1 (Th1) response and reduces the expression of major histocompatibility complex II (MHC-II) and interferon-gamma receptors (IFNGRs). Here we will review some studies to provide a paradigm for the induction, regulation, and role of IFN-beta in mycobacterial infection. Indeed, recent studies suggest that IFN-beta plays a role in Mtb survival in host cells and its downregulation may be a useful therapeutic strategy to control Mtb infection.