Nontuberculous mycobacterial (NTM) are found ubiquitously in the environment and are usually of low pathogenicity. Infection occurs via inhalation of aerosols, and some species may cause severe infections. The incidence of NTM infections is rising worldwide. The risk of developing NTM disease depends on the susceptibility of the host as well as the frequency and duration of exposure. In addition to congenital immune deficiencies and immunosuppressive therapy, structural lung and systemic diseases, including rheumatoid arthritis (RA), are associated with an increased risk for NTM infections. The immune response to NTM is complex and relies on the interplay between professional phagocytes and lymphoid cells. This interplay is concerted by three key cytokines: interleukin-12 (IL-12), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ). Targeted immunotherapies, e. g., treatment with TNF inhibitors, interfere with these essential pathways and increase the risk of NTM infection significantly. This review focuses on the relationship between the immune response to NTM and intrinsic and iatrogenic dispositions for NTM infection, with an emphasis on RA.
Keywords: Immunotherapy; Interferon-γ; Interleukin-12; Rheumatoid arthritis; Tumor necrosis factor-α.