title: Regulation of T cells in asthma: implications for genetic manipulation.
abstract: OBJECTIVE
  Allergic asthma is a disease characterized by airway hyperresponsiveness, inflammation and remodeling. In the past few decades it has become clear that the pathogenesis and development of this disease is controlled by cytokines released by CD4 T helper type 2 lymphocytes that develop under the influence of natural killer lymphocytes. At birth, T cell priming exhibits a T helper type 2 bias and the development of the T helper phenotype is determined in the first year of life by environmental exposure to virus or bacterial substances or environmental allergens in genetically predisposed individuals. Decreased exposure to infection in early childhood has thus been linked to the increased incidence of asthma in industrialized countries (hygiene hypothesis). In this review, we discuss the possibility that the kind and the quantity of infectious agent determines the type of immune response.
  
  
  RESULTS
  It has previously been shown that Toll-like receptors are involved in the recognition of intermediate components, which is the result of processed foreign antigens or damage products (produced during infection, damage or inflammation). In addition, the protective effect against allergic diseases is mediated by a new subset of CD4 T cells: the T-regulatory cells.
  
  
  CONCLUSIONS
  The kind and dose of antigen or infectious agent determines the development of a T helper type 1 or type 2 immune response and the activation of T-regulatory cells. The latter are known to play an important role in downregulating allergic immune responses.
authors.affiliation: I Medical Clinic, University of Mainz, Mainz, Germany.
authors.forename: Cornelia
authors.initials: C
authors.lastname: Luft
authors.forename: Michael
authors.initials: M
authors.lastname: Hausding
authors.forename: Susetta
authors.initials: S
authors.lastname: Finotto
mesh_terms: D001249:Asthma / Q000235:genetics / Q000276:immunology* / Q000503:physiopathology*; D016207:Cytokines / Q000235:genetics / Q000276:immunology / Q000502:physiology; D006801:Humans; D008070:Lipopolysaccharides / Q000276:immunology; D008562:Membrane Glycoproteins / Q000235:genetics / Q000276:immunology / Q000502:physiology; D011956:Receptors, Cell Surface / Q000235:genetics / Q000276:immunology / Q000502:physiology; D020825:T-Box Domain Proteins; D013601:T-Lymphocytes / Q000276:immunology / Q000502:physiology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology / Q000502:physiology; D051193:Toll-Like Receptors; D014157:Transcription Factors / Q000235:genetics / Q000276:immunology / Q000502:physiology; D000098815:T-bet Transcription Factor
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; D020825:T-Box Domain Proteins; D000098815:T-bet Transcription Factor; D051193:Toll-Like Receptors; D014157:Transcription Factors