title: Future treatments of allergic diseases and asthma.
abstract: Recent advances in the understanding of the inflammatory and immunological mechanisms of allergic diseases have illuminated many potential therapeutic strategies that may prevent or even reverse the abnormalities of allergic inflammation. As the roles of effector cells, and of signalling and adhesion molecules are better understood, the opportunities to inhibit or prevent the inflammatory cascade have increased. In addition, there have been advances in the synthesis of proteins, monoclonal antibodies and new small molecule chemical entities, which provide further valuable flexibility in the therapeutic approach to asthma. Such new approaches are aimed at prevention of T-cell activation; redressing the imbalance of T helper cell populations thus inhibiting or preventing Th-2-derived cytokine expression; and the inhibition or blockade of the downstream actions of these cytokines such as effects on IgE and eosinophils. Approaches such as these allow both broad and highly specific targeting, and may pave the way towards the prevention and reversal of the immunological and inflammatory processes driving asthma, allergic rhinitis and atopic dermatitis. The development of effective agents with effects beyond those provided by current therapies coupled with lesser side-effects will further address the unmet needs of allergic disease.
authors.affiliation: National Heart & Lung Institute, Imperial College School of Medicine and Royal Brompton Hospital, London, UK.
authors.forename: R G
authors.initials: RG
authors.lastname: Stirling
authors.forename: K F
authors.initials: KF
authors.lastname: Chung
mesh_terms: D000276:Adjuvants, Immunologic / Q000627:therapeutic use*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001249:Asthma / Q000276:immunology / Q000628:therapy; D015704:CD4 Antigens / Q000276:immunology; D016207:Cytokines / Q000008:administration & dosage; D004804:Eosinophils / Q000276:immunology; D005544:Forecasting; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology / Q000628:therapy*; D007073:Immunoglobulin E / Q000276:immunology; D007375:Interleukin-1 / Q000037:antagonists & inhibitors; D016753:Interleukin-10 / Q000037:antagonists & inhibitors; D008213:Lymphocyte Activation; D051379:Mice; D013601:T-Lymphocytes / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors; D014611:Vaccination
chemical_list: D000276:Adjuvants, Immunologic; D000911:Antibodies, Monoclonal; D015704:CD4 Antigens; D016207:Cytokines; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007073:Immunoglobulin E