Innate immunity to TB: a druggable balancing act.
editorial · Level V
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- Record sourced from PubMed, PMID 22304907.
- Also identified by DOI 10.1016/j.cell.2012.01.026.
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Abstract
Tobin and colleagues show that both inhibition and excessive production of the inflammatory mediator TNFα impact the pathogenesis of tuberculosis (TB) and the response to therapy. Identifying a critical role for the genetically determined balance between pro- and anti-inflammatory eicosanoids in regulating TNFα levels provides a roadmap to tailored TB treatment based on host genotype.