Old friends for breakfast.
These workers suggest that the hygiene hypothesis, although essentially correct, has spawned 3 untenable interpretations that delayed its acceptance. First the suggestion that diminished exposure to microorganisms fails to drive Th1 cells, with a consequent overproduction of Th2 cells. It is now clear that the critical balance is not Th1/Th2 but rather regulatory T cells (Treg)/Teffector. Secondly, the suggestion that we must suffer infections such as TB or childhood virus infections, in order to be protected from chronic inflammatory disorders. This view has little epidemiological support, and several studies have shown that these infections do not protect from allergies. Thirdly, there was the view, largely created by the media, that home hygiene itself is in some way to blame. Again, a detailed recent report has rejected this simplistic concept. Rook and Brunet suggest that the answer lies in the ‘Old Friends' mechanism. Certain harmless micro-organisms that are part of our evolutionary history are recognized as ‘Old Friends' by the innate immune system; hence, rather than priming aggressive immune responses, they prime immunoregulation, mediated in part by release of IL-10 and transforming growth factor (TGF)-b. Rook and Brunet speculate that stimulation of innate immunity with components of saprophytic mycobacteria, lactobacilli and certain helminths (the ‘Old Friends') will form the basis of treatment in the future by driving both specific and bystander immunoregulation. Clinical and Experimental Allergy 2005; 35: 841-842.
Publication Type: Journal article
Publisher: Clinical and Experimental Allergy