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The Timothy grass allergen-specific T-cell receptor (TCR) is a specialized protein complex on the surface of CD4+ T cells that mediates the immune system's response to Phleum pratense pollen (Wambre et al., 2011) [4]. It functions by recognizing specific peptide fragments from major allergens, such as Phl p 1 and Phl p 5, when they are presented by Major Histocompatibility Complex (MHC) Class II molecules on antigen-presenting cells (Schulten et al., 2013) [13]. In sensitized individuals, this recognition event initiates a Th2-biased inflammatory cascade, characterized by the release of cytokines like IL-4, IL-5, and IL-13, which drive IgE production and allergic symptoms (Schenk et al., 1995) [9]. Therapeutic strategies, primarily allergen-specific immunotherapy (AIT) such as Grastek or Grazax, target these TCRs by delivering controlled doses of the allergen to reprogram the immune response (FDA, 2014) [17]. This modulation leads to the induction of regulatory T cells (Tregs) and the production of protective IgG4 antibodies, ultimately resulting in long-term clinical tolerance and reduced sensitivity to grass pollen (O'Brien et al., 2013) [7].
Allergen-specific immunotherapy (AIT) modulates the T-cell receptor response by inducing peripheral tolerance, promoting the development of regulatory T cells (Tregs), and shifting the cytokine profile from a Th2-biased allergic response to a Th1/Treg-mediated tolerant state, often accompanied by the production of allergen-specific IgG4 blocking antibodies.
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