Th-1/Th-2 Switch Regulation in Immune Responses to Inhaled Antigens

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Until comparatively recently, allergic (atopic) disease was viewed as a manifestation of hyperreactivity to essentially non-pathogenic soluble protein antigens which are ubiquitous in the natural environment. In this context, normality would equate to non-responsiveness, resulting from either tolerance or ignorance of the antigens. However, it is now clear (reviewed inc[1]) that active T cell immunity to at least one class of these antigens (airborne ”inhalant“ allergens) is essentially universal amongst adults, clinical reactivity being a function of the cytokine profiles of CD4+ Th-cells which dominate relevant Th-memory populations. Thus, atopics who respond to allergen exposure via IgE production, eosinophilia etc., manifest Th-2-skewed memory, whereas T cell memory in non-responsive normal adults is dominated by Th- I -cytokines such as IFNγ. The situation with respect to ingested environmental allergens (ubiquitous in the diet) appears both qualitatively and quantitatively different, as T cell reactivity to this class of antigens is considerably less frequent in the adult population1.2.