RESUMEN
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.
Asunto(s)
Artritis Reumatoide/complicaciones , Síndromes de Inmunodeficiencia/complicaciones , Inmunosupresores/efectos adversos , Infecciones por Mycobacterium no Tuberculosas/diagnóstico , Infecciones Oportunistas/diagnóstico , Artritis Reumatoide/inmunología , Artritis Reumatoide/terapia , Humanos , Enfermedad Iatrogénica , Síndromes de Inmunodeficiencia/inmunología , Síndromes de Inmunodeficiencia/terapia , Inmunoterapia , Interferón gamma/sangre , Interleucina-12/sangre , Linfocitos/inmunología , Infecciones por Mycobacterium no Tuberculosas/epidemiología , Infecciones por Mycobacterium no Tuberculosas/inmunología , Infecciones por Mycobacterium no Tuberculosas/terapia , Infecciones Oportunistas/epidemiología , Infecciones Oportunistas/inmunología , Infecciones Oportunistas/terapia , Fagocitos/inmunología , Factores de Riesgo , Factor de Necrosis Tumoral alfa/sangreRESUMEN
Infections with Mycobacterium tuberculosis (MTB) induce complex immune responses involving an orchestrated interplay of innate and adaptive immune mechanisms. Why the immune system fails to eradicate the pathogen and at best achieves control of infection in the latent stage, still remains an unsolved mystery even more than 100 years after the discovery of MTB by Robert Koch. This article provides an overview of the current state of the art in the constantly evolving field of tuberculosis (TB) immunology. This review focuses on a change of paradigm proposing that in the latent stage MTB is anything but dormant and that latent TB is not merely a state of bacterial stasis but a state of dynamic bacterial and immunological equilibrium. The understanding of these dynamics is crucial for the development of new drugs against MTB as well as vaccines that aim to provide effective protection against the disease.