Journal
CELL
Volume 148, Issue 3, Pages 389-391Publisher
CELL PRESS
DOI: 10.1016/j.cell.2012.01.026
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Tobin and colleagues show that both inhibition and excessive production of the inflammatory mediator TNFa 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 TNFa levels provides a roadmap to tailored TB treatment based on host genotype.
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