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The T-cell receptor (TCR) recognizing Amb a 1-derived peptides is a critical mediator of the allergic immune response to short ragweed (Ambrosia artemisiifolia). Amb a 1 is the primary allergen in ragweed pollen, and its peptides are processed and presented by Major Histocompatibility Complex (MHC) class II molecules on antigen-presenting cells (Wopfner et al., 2005). When these peptide-MHC complexes bind to specific TCRs on CD4+ T cells, they trigger a Th2-polarized immune response characterized by the production of cytokines like IL-4, IL-5, and IL-13 (Jahn-Schmid et al., 2005). This cascade leads to IgE production by B cells and the subsequent clinical symptoms of allergic rhinitis and asthma (Gadermaier et al., 2004). Therapeutic strategies targeting this interaction include allergen-specific immunotherapy (AIT), which aims to induce immune tolerance or desensitization by repeatedly exposing the TCR to the allergen or its derivative peptides (Creticos et al., 2006). Such treatments seek to shift the immune profile toward a Th1 or regulatory T-cell (Treg) response, thereby reducing allergic inflammation (Worm et al., 2011).
Induction of immunological tolerance through T-cell anergy, clonal deletion, or immune deviation from a Th2-type response to a Th1 or regulatory T-cell (Treg) profile (Creticos et al., 2006; Jahn-Schmid et al., 2005).
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