Abstract
A third of the world’s population is exposed to Mycobacterium tuberculosis in their lifetime. Over eight million people develop a tuberculosis (TB) illness and 1.3 million people die from the disease every year. Acquired immunity (cytotoxic CD8+ T cells (CBT), Th1 CD4+ helper T cells) macrophages, and dendritic cells all play important roles in TB infection. Recently, it is well established that innate immunity as well plays a definitive role in the development of TB immunity under the effects of several cytokines, microbicidal proteins and Toll-like receptors. Meanwhile, the introduction and widespread use of biological disease-modifying anti-rheumatic reagents over the last 15 years worldwide has dramatically advanced and improved the standard care and prognosis of patients with rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA).However, as clinical experience with these drugs has grown, the risk of granulomatous infections, especially disseminated TB and fungal infections, has become apparent, especially because having RA or JIA may innately increase the risk of infection (bacterial, viral and fungal). The knowledge of basic immunology has also advanced over the past 10 years and adult and pediatric rheumatologists should increase their understanding of this dynamic between arthritis diseases, anti-TNF- α medications, and TB. This review will provide an up-to-date discussion of both the immunology of the TB organism in the human host and the pathophysiologic mechanisms of the TNF-α blockers in the development of secondary (disseminated) tuberculosis.
Highlights
Biological reagents (so-called “biologics”) target cytokines and cell surface proteins
Biological reagents target cytokines and cell surface proteins
Using data collected from the adverse event reporting system of the FDA, Wallis found an increase in other granulomatous infections associated with infliximab compared with etanercept (54 versus 32 cases per 100,000 patients treated; p < 0.001) [4]
Summary
Biological reagents (so-called “biologics”) target cytokines and cell surface proteins. TNF-α promotes the maturation of monocytes to dendritic cells (DCs) and/or macrophages, inducing the antigen presentation of intracellular mycobacteria. The activated CTL cells have the ability to produce perforin protein and TNF-α by itself, which guide TB-infected monocytes to apoptosis, which involves intracellular living TB bacilli, and to induce the autophagy of infected cells via activated macrophages [20] (Figure 3).
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