Background: Allergic inflammation is considered to be the result of a pattern of Th2 lymphocyte activation. However this inflammation, relevant for atopy and infiltration of affected tissues by eosinophils, is insufficient by itself to explain the clinical features of asthma. Several studies have demonstrated that Th2 type inflammation was also associated in asthma with a Th1 response, with production of gamma interferon. It has recently been shown that the regulatory T lymphocytes (Treg) which produce IL-10 and/or TGF-beta and induce tolerance are defective in allergic patients. In addition, these lymphocytes increase during specific immunotherapy. Their decrease could explain the Th2 activation found in atopic patients.
Perspective: We review the potential importance of Treg cells in atopy and also asthma, and propose a concept whereby the allergic inflammatory response would not be due to a Th1/Th2 imbalance, but rather to a Treg deficiency progressively rising from normal to atopic, from atopy to asthma and from asthma to acute exacerbations.
Conclusion: Three dimensions of inflammation need therefore to be taken into account: Th1, Th2 and Treg.