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The T cell receptor (TCR) on Bet v 1-specific CD4+ T cells is the primary molecular sensor responsible for initiating the allergic immune response to birch pollen. These receptors recognize specific peptide fragments of the major birch allergen, Bet v 1, when presented by Major Histocompatibility Complex (MHC) class II molecules on the surface of antigen-presenting cells (1.1.3, 1.3.4). In sensitized individuals, the activation of these TCRs typically leads to a Th2-polarized response, characterized by the secretion of pro-inflammatory cytokines such as IL-4, IL-5, and IL-13, which drive IgE production and allergic inflammation (1.3.3, 1.3.5). This TCR is a major therapeutic target for allergen-specific immunotherapy (AIT), which aims to reprogram the immune system toward tolerance (1.1.1, 1.3.2). Therapeutic strategies involve the administration of controlled doses of Bet v 1 or its peptides to induce T cell anergy, exhaustion, or the differentiation of regulatory T cells (Tregs) that suppress the allergic cascade (1.2.1, 1.3.2). Furthermore, because Bet v 1 shares structural homology with proteins in various fruits and nuts, these TCRs often exhibit cross-reactivity, contributing to the development of pollen-food allergy syndrome (1.1.2, 1.4.1).
Allergen-specific immunotherapy (AIT) targets these TCRs by providing repeated, controlled exposure to the Bet v 1 allergen or its immunodominant peptides. This process induces immune tolerance through several mechanisms: the induction of T cell anergy or deletion, immune deviation from a Th2 to a Th1 response, and the expansion of regulatory T cells (Tregs) that secrete suppressive cytokines like IL-10 and TGF-beta to inhibit allergic inflammation.
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