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a San Raffaele
Institute, 20132 Milan, Italy, b G Gaslini Institute, Genoa, Italy
Correspondence to: Dr S E Burastero.
Received 20 November 1998; Returned to authors 8 December 1998; Revised version received 19 January 1999; Accepted for publication 26 January 1999
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Introduction |
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In allergic asthma, allergen specific T lymphocytes of the CD4 subset (T helper or Th cells) control the cellular and molecular events underlying the establishment and chronic maintenance of airway inflammation that characterises the disease. The basic immunological event is the shift of allergen reactive CD4 Th lymphocytes towards a Th2 phenotype with the production of Th2 cytokines such as interleukin (IL)-4, IL-13, and IL-5. Th2 cells can support both allergen specific IgE production and eosinophil recruitment.
Recognition of allergen via the T cell receptor (TcR) provides the
trigger for a specific T cell response; as any antigen, allergen is
seen by Th cells as one of a few possible peptides derived from
proteolytic processing. Immunogenic peptides are presented on major
histocompatibility complex (MHC) molecules expressed on the membrane of
antigen presenting cells. However, antigen recognition can follow such
opposite events as anergy or activation of T cells
that is,
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