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The T-cell receptor (TCR) recognizing Phleum pratense-derived peptides presented by HLA class II is a key molecular complex in the development of Timothy grass allergy. These receptors are expressed on the surface of CD4+ T lymphocytes and specifically bind to allergenic peptides, such as those from Phl p 1 and Phl p 5, when they are displayed by MHC class II molecules on antigen-presenting cells [1.1.1, 1.2.1]. In sensitized individuals, this binding event initiates a Th2-biased immune cascade, leading to the production of allergen-specific IgE and the recruitment of effector cells like mast cells and eosinophils [1.3.2, 1.4.4]. This process is responsible for the clinical symptoms of allergic rhinitis and asthma upon exposure to grass pollen [1.4.3, 1.5.4]. Therapeutic interventions, most notably allergen-specific immunotherapy (AIT), target this pathway by exposing the immune system to controlled amounts of the allergen [1.4.1, 1.5.1]. The goal of such therapy is to induce peripheral T-cell tolerance, characterized by the induction of regulatory T cells (Tregs) and a shift from a Th2 to a Th1 cytokine profile [1.3.4, 1.3.5]. Successful modulation of these TCR-mediated responses results in long-term desensitization and a reduction in allergic inflammation [1.4.3].
Induction of peripheral T-cell tolerance through regulatory T-cell (Treg) expansion, Th2-to-Th1 cytokine shift, and production of IgG4 blocking antibodies.
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