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House dust mite-specific T helper 2 (Th2) cells are a specialized subset of CD4+ T lymphocytes that play a central role in the pathogenesis of allergic diseases such as asthma and rhinitis (Wambre et al., 2017, Science Translational Medicine). These cells possess T-cell receptors (TCRs) that specifically recognize peptide fragments derived from house dust mite (HDM) allergens, such as Der p 1 and Der p 2, when presented by Major Histocompatibility Complex (MHC) class II molecules on antigen-presenting cells (Robinson et al., 2004, Journal of Allergy and Clinical Immunology). Upon activation, these allergen-specific Th2 cells secrete pro-inflammatory cytokines, including IL-4, IL-5, and IL-13, which drive IgE production by B cells and recruit eosinophils to the airways (Larche et al., 2006, Nature Reviews Immunology). In allergic individuals, a distinct phenotype known as Th2A cells (CD27- CD45RB- CRTH2+) has been identified as the primary driver of this allergic response. Therapeutic strategies targeting these cells include allergen-specific immunotherapy (AIT), such as Odactra or Acarizax, which aim to induce immune tolerance by shifting the T-cell response toward a regulatory (Treg) or Th1 phenotype (FDA, 2017). Additionally, peptide-based vaccines like HDM-SPIRE are designed to target the TCR-pMHC interaction directly to induce anergy or deletion of these pathogenic cells without the risk of IgE-mediated anaphylaxis. Monitoring these cells using pMHC tetramers serves as a critical biomarker for evaluating the efficacy of desensitization treatments in clinical settings.
Induction of immune tolerance through T-cell anergy, clonal deletion, or immune deviation from a pro-inflammatory Th2 phenotype to a regulatory T-cell (Treg) or Th1 phenotype.
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