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, induction of tolerance versus establishment of an effective immune response. Current concepts recognise that the outcome of antigen recognition is dependent, at least in part, on the complex interaction between MHC molecule associated membrane proteins (collectively known as co-stimulatory molecules) on the antigen presenting cells and their ligands on the T cells. Moreover, when the immune response is activated, co-stimulation is also involved in determining which effector profile will be acquired by the T cells—that is, a Th1 or a Th2 phenotype.

We will briefly review the experimental evidence supporting the concept that interference with the proper co-stimulatory molecules may allow the design of pharmaceutical products which cause immune deviation that could quantitatively and qualitatively change the T cell response. This approach could interfere with the chronic amplification of allergic inflammation at the level of the target organ in atopic individuals.