Regulatory T-cell responses in patients with type I allergies

It is well established that IgE antibodies (Abs) to allergens are the predominant and most likely the only isotype of Abs responsible for inducing type I allergic diseases in humans. However, not all individuals exposed to allergens become allergic and moreover, not all individuals with elevated IgE Abs to exogenous antigens show immediate hypersensitivity reactions to these antigens. Although it is well established that offspring of atopic parents are at increased risk of developing atopy, debate still persists over the pattern of inheritance. IgE production is T-cell dependent of surface signalling molecules, as well as the soluble factors interleukin-4(IL-4) and IL-13. However, the exact mechanisms and molecules involved in the regulation of IgE synthesis are far from being understood.
Recently we have shown that early exposure to Epstein-Barr and cytomegalovirus seems to protect against the development of early atopy. One early key cell involved in protection against viruses is NK cells. The role of NK cells in the development of early atopy is not known
This proposed research addresses the dissection of the regulatory mechanisms involved in the pathogenesis of type I allergic diseases with special emphasis on: 1) elucidating at the cellular and molecular level, the mechanism(s) behind the switching to IgG4 and IgE production in allergic and non-allergic individuals; 2) investigating how allergen-specific T-cell responses are influenced by maternally derived host factors in children developing atopy and delivered by mothers with or without atopy; and 3) to investigate the role of NK cells in the development of early atopy

People involved in this project: PhD Yvonne Sundström