“…Whereas IFN-g and TNF can be produced by innate immune cells, T cells are potent producers of these cytokines and have been shown to be critical for controlling mycobacterial infection in animal models and humans (Szabo et al 2003;Al-Muhsen and Casanova 2008;Kwan and Ernst 2011;Philips and Ernst 2012;Tubo and Jenkins 2014). Mice deficient in CD4 þ T cells, IFN-g signaling, or TNF signaling show disorganized macrophage aggregates that become necrotic (Kindler et al 1989;Flynn et al 1993Flynn et al , 1995Bean et al 1999;Caruso et al 1999;Scanga et al 2000;Flynn and Chan 2001;Roach et al 2002;Algood et al 2005;Stenger 2005;Chakravarty et al 2008;Wallis and Schluger 2010). These observations associated granuloma formation with a protective immune response to TB.…”
Section: Summary: a New Role For The Granuloma From A Historical Persmentioning
“…In conceptualizing how these agents predispose to NTM infections, it is important to understand that, whereas anti-TNFα antibody agents and etanercept are roughly equally effective against rheumatoid arthritis, psoriasis, and ankylosing spondylitis, etanercept is not very effective against disorders such as Crohn disease and sarcoidosis, which are characterized by granulomatous pathology. 66 This observation may be related to why etanercept appears to confer a lower risk of granulomatous infectious complications than the anti-TNF-α neutralizing antibodies.  Variations in mechanisms of action of these two drug categories may help explain why anti-TNF-α antibodies are more likely to be associated with opportunistic infections than etanercept (►Fig.…”
Section: Tnf-α Antagonistsmentioning
“…66 This observation may be related to why etanercept appears to confer a lower risk of granulomatous infectious complications than the anti-TNF-α neutralizing antibodies.  Variations in mechanisms of action of these two drug categories may help explain why anti-TNF-α antibodies are more likely to be associated with opportunistic infections than etanercept (►Fig. 5).…”
Nontuberculous mycobacteria (NTM) are environmental microbes that cause a variety of human diseases, particularly chronic lung infections. Despite the fact that NTM are widespread in the environment, relatively few people develop NTM lung disease, suggesting intrinsic vulnerability in some individuals. This paper reviews the evidence that underlying disorders predispose to NTM lung disease, in particular primary conditions that result in bronchiectasis, chronic obstructive pulmonary disease, α-1-antitrypsin anomalies, pneumoconiosis, pulmonary alveolar proteinosis, and frank immunosuppressive states such as that associated with the use of anti-tumor necrosis factor-α biologics, posttransplantation immunosuppression, and HIV infection. Over the past several decades, NTM lung disease has been increasingly identified in postmenopausal women with slender body habitus. Thus we will also review the clinical and experimental evidence which supports the observation that such individuals are predisposed to NTM lung disease.
“…7 However, in recent years, other potent classes of immunosuppressive therapies have been developed, and use of these therapies, most notably highly potent tumor necrosis factor-α (TNF-α) inhibitors such as infliximab and adalimumab, has been associated with a greatly increased risk of progression from latent to active disease.  Patients being treated with these therapies are also important candidates for testing and treatment of latent infection.…”
Section: Testing For Latent Tuberculosis Infection In Immunocompromismentioning
Accurate diagnosis of tuberculosis (TB) infection is an important component of tuberculosis control programs in many countries. Identification of persons with asymptomatic, or latent, tuberculosis infection allows for treatment of individuals at high risk for progressing to active disease so that the overall burden of tuberculosis disease is diminished. In the United States, targeted testing and treatment of latent tuberculosis infection (LTI) are major components of the Centers for Disease Control and Prevention's efforts at TB elimination. This review focuses on the comparative utility of tuberculin skin testing and interferon-gamma release assays (IGRAs) to diagnose LTI. Commercially available IGRAs have superior sensitivity and specificity compared with conventional tuberculin skin testingin some settings (particularly bacille-Calmette Guérin-vaccinated individuals). Also discussed are the performance characteristics of these tests in specific populations, including foreign-born persons from high-prevalence countries, close contacts of actively infected patients, immunocompromised populations, and health care workers.
A wide array of bacteria, viruses, fungi and protozoa may cause severe pulmonary infectious diseases in patients with primary immunodeficiency and patients on treatment with anti-TNF and anti-CD20 drugs. Knowledge of the association of certain microbial agents with specific immune disturbances is of great clinical interest.
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