The Role of RIG-I-Like Receptors in the Activation of Innate Immune in Tuberculosis

Abstract

Tuberculosis still claims over a million lives every year. The infection process can be regarded as an imbalance between the immune response and Mycobacterium tuberculosis growth. To successfully survive in an infected organism, M. tuberculosis must overcome the mechanisms of innate immunity, including those aimed at recognition of pathogen nucleic acids. RIG-I-like receptors (RLRs) is a system of intracellular sensors of foreign RNA, which is involved in the recognition of viruses and bacterial pathogens. RIG-I, MDA5, and LGP2 receptors interact directly with RNA in the cell cytoplasm and trigger a cascade of interactions leading to the synthesis of type I interferons and pro-inflammatory cytokines. To date, it has been proven that RLR activation during tuberculosis is among the most important components of innate immunity. Their role in the activation of type I interferons is undoubted, however, can be not only protective, but also detrimental. The review considers the latest data on the RLRs functioning in M. tuberculosis infection.