Anti-tumor necrosis factor-α (TNF-α) biological agents, including soluble TNF-α receptors and anti-TNF-α monoclonal antibodies, bring new hope for treating rheumatic diseases such as rheumatoid arthritis, but also increase the risk of infection, especially tuberculosis (TB) infection. Recent findings have shown that the physiological TNF-mediated signaling was somehow impaired by TNF antagonists, leading to the exacerbation of chronic infection associated with aberrant granuloma formation and maintenance. Although both receptor and antibody agents appear to pose an equally high risk in causing development of new TB infections, monoclonal anti-TNF-α antibody seems more inclined to reactivate latent TB infection. This review is focused on the underlying mechanisms that cause the TB risk in the anti-TNF-α therapy and also the strategies to deal with it, with the aim of reducing the TB incidence during anti-TNF-α biological therapies.
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| http://dx.doi.org/10.1016/j.jmii.2013.03.005 | DOI Listing |
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