title: Tregs and allergic disease.
abstract: Allergic diseases such as asthma, rhinitis, and eczema are increasing in prevalence and affect up to 15% of populations in Westernized countries. The description of Tregs as T cells that prevent development of autoimmune disease led to considerable interest in whether these Tregs were also normally involved in prevention of sensitization to allergens and whether it might be possible to manipulate Tregs for the therapy of allergic disease. Current data suggest that Th2 responses to allergens are normally suppressed by both CD4+CD25+ Tregs and IL-10 Tregs. Furthermore, suppression by these subsets is decreased in allergic individuals. In animal models, Tregs could be induced by high- or low-dose inhaled antigen, and prior induction of such Tregs prevented subsequent development of allergen sensitization and airway inflammation in inhaled challenge models. For many years, allergen-injection immunotherapy has been used for the therapy of allergic disease, and this treatment may induce IL-10 Tregs, leading to both suppression of Th2 responses and a switch from IgE to IgG4 antibody production. Improvements in allergen immunotherapy, such as peptide therapy, and greater understanding of the biology of Tregs hold great promise for the treatment and prevention of allergic disease.
authors.affiliation: Department of Allergy and Clinical Immunology, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, United Kingdom.
authors.forename: Douglas S
authors.initials: DS
authors.lastname: Robinson
authors.forename: Mark
authors.initials: M
authors.lastname: Larché
authors.forename: Stephen R
authors.initials: SR
authors.lastname: Durham
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control / Q000628:therapy; D001327:Autoimmune Diseases / Q000517:prevention & control; D015704:CD4 Antigens / Q000276:immunology; D004195:Disease Models, Animal; D004485:Eczema / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control / Q000628:therapy; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology / Q000517:prevention & control; D007167:Immunotherapy; D007249:Inflammation / Q000276:immunology / Q000517:prevention & control; D016753:Interleukin-10 / Q000276:immunology; D008213:Lymphocyte Activation; D008954:Models, Biological; D010446:Peptide Fragments / Q000276:immunology / Q000627:therapeutic use; D015375:Receptors, Interleukin-2 / Q000276:immunology; D012220:Rhinitis / Q000276:immunology* / Q000473:pathology / Q000517:prevention & control / Q000628:therapy; D016176:T-Lymphocyte Subsets / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000485:Allergens; D015704:CD4 Antigens; D010446:Peptide Fragments; D015375:Receptors, Interleukin-2; D016753:Interleukin-10