page 1199. Parasitic helminth infections, they show, activate regulatory T (T reg) cells in the gut. These T reg cells are then dispatched to the lungs, where they dampen the immune response to inhaled allergens.
Parasitic worm infections, common among children in tropical and subtropical regions, are associated with decreased responsiveness to allergens. The hygiene hypothesis, which posits that decreased childhood exposure to T helper (Th) 1–inducing microbes (such as bacteria and viruses) increases the risk of developing Th2-driven allergies later in life, might explain this observation. But the allergy-soothing effect of worm infections is unlikely to be due to Th1–Th2 antagonism, as both helminth infections and allergies induce potent Th2 responses.Wilson and colleagues now show that mice infected with an intestinal helminth had decreased airway inflammation and Th2 effector cytokine production in response to inhaled allergens, as compared with uninfected mice. T reg cells developed in response to the worm infection—possibly a tactic developed by the parasite to avoid immune expulsion. These cells were the culprits behind the worm-induced allergy suppression, as uninfected mice given T reg cells from infected mice were rendered similarly allergy-resistant.
The authors are now investigating how chronic worm infections trigger T reg cell responses. In the meantime, the hygiene hypothesis may need refinement, as increased allergic responses might result more from a paucity of T reg cells than from diminished Th1 responses.