title: Targeting Th2 cells in asthmatic airways.
abstract: The most effective anti-asthmatic drugs currently available include inhaled beta2-agonists and glucocorticoids and control asthma in about 95% of patients. The current asthma therapies are not cures and symptoms return soon after the treatment is stopped even after long-term therapy. In addition, severe glucocorticoid-dependent and -resistant asthma still represents a great clinical burden accounting for approximately 50% of the health care costs of asthma and reducing the side-effects of glucocorticoids using novel dissociated steroids, soft steroids or with steroid-sparing agents will prove beneficial. Furthermore, the mechanisms involved in the persistence of inflammation are poorly understood and the reasons why some patients have severe life threatening asthma and others have very mild disease are still unknown. Hopefully, it will soon be possible to identify and manipulate the molecular switches that result in asthmatic inflammation. This may lead to the treatment of susceptible individuals at birth or in the early years and thus prevent the disease from becoming established. Drug development for asthma has been directed at improving currently available drugs and finding new compounds that usually target the Th2-driven airway inflammatory response. Several new drugs have been developed to target specific components of the Th2-driven inflammatory process in asthma (e.g. IgE antibodies, cytokines and/or chemokines, immunomodulators, antagonists of adhesion molecules), although they have not yet been proven to be particularly effective. Some of these new Th2-oriented strategies may in the future not only control symptoms, but also potentially prevent or cure the disease.
authors.affiliation: Dipartimento di Medicina Clinica e Sperimentale, Centro di Ricerca su Asma e BPCO, Università di Ferrara, Italy. crm@unife.it
authors.forename: Gaetano
authors.initials: G
authors.lastname: Caramori
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Ito
authors.forename: Ian M
authors.initials: IM
authors.lastname: Adcock
mesh_terms: D015105:3',5'-Cyclic-AMP Phosphodiesterases / Q000037:antagonists & inhibitors; D000818:Animals; D018927:Anti-Asthmatic Agents / Q000494:pharmacology / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology; D018925:Chemokines / Q000378:metabolism; D054703:Cyclic Nucleotide Phosphodiesterases, Type 4; D006801:Humans; D007167:Immunotherapy / Q000379:methods; D019707:Receptors, Chemokine / Q000037:antagonists & inhibitors / Q000276:immunology; D013602:T-Lymphocytes, Cytotoxic / Q000187:drug effects / Q000276:immunology; D018417:Th1 Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D018418:Th2 Cells / Q000187:drug effects* / Q000276:immunology; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D018927:Anti-Asthmatic Agents; D018925:Chemokines; D019707:Receptors, Chemokine; D014157:Transcription Factors; D015105:3',5'-Cyclic-AMP Phosphodiesterases; D054703:Cyclic Nucleotide Phosphodiesterases, Type 4