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The World Health Organization estimates that a third of the world’s population is infected with tuberculosis (TB). In approximately 90% of people, the infection remains latent. In others, TB disease develops, often in the first two years after infection. Individuals whose immune systems are compromised by disease or drugs are at increased risk for developing TB disease.
The pathogenesis of TB is complex. In pulmonary TB, inhaled TB bacilli are first engulfed by alveolar macrophages. Next, they replicate and briefly disseminate haematogenously throughout the body. The host attempts to limit bacilli spread with granuloma formation, a process mediated by tumour necrosis factor (TNF) α.1,2 This proinflammatory cytokine is released by activated immune cells. It mediates systemic inflammatory responses and tissue destruction, and is important in the pathogenesis of autoimmune diseases such as rheumatoid arthritis, psoriasis, and Crohn’s disease.
Recently, TNFα blocking drugs (infliximab, etanercept, and adalimumab) have been shown to be highly successful in the treatment of the above mentioned autoimmune diseases and other conditions. However, infectious complications have been reported with all three drugs including the reactivation of latent TB infection, which …