The mechanisms involved are not yet fully delineated but induction of IFNγ+Tbet+CD8+ T cells appears to play a key role and indeed, ES-62’s protective actions are blocked by administration of neutralising anti-IFNγ antibodies suggesting that the parasite product acts to homeostatically reset the Th cell balance in this acute airway inflammation model6, 8. The gene discussed is IFNG; the disease is inflammation.