Update on tuberculosis and other opportunistic infections associated with drugs blocking tumour necrosis factor α

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Abstract
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.