Allergy, Parasites, and the Hygiene Hypothesis

Abstract

The increase of allergic diseases in the industrialized world has often been explained by a decline in infections during childhood. The immunological explanation has been put into the context of the functional T cell subsets known as T helper 1 (T H 1) and T helper 2 (T H 2) that display polarized cytokine profiles. It has been argued that bacterial and viral infections during early life direct the maturing immune system toward T H 1, which counterbalance proallergic responses of T H 2 cells. Thus, a reduction in the overall microbial burden will result in weak T H 1 imprinting and unrestrained T H 2 responses that allow an increase in allergy. This notion is contradicted by observations that the prevalence of T H 1-autoimmune diseases is also increasing and that T H 2-skewed parasitic worm (helminth) infections are not associated with allergy. More recently, elevations of anti-inflammatory cytokines, such as interleukin-10, that occur during long-term helminth infections have been shown to be inversely correlated with allergy. The induction of a robust anti-inflammatory regulatory network by persistent immune challenge offers a unifying explanation for the observed inverse association of many infections with allergic disorders.