T-cell receptor recognizing house dust mite allergens (HDM-specific TCR)

T-cell receptors (TCRs) that specifically recognize peptides derived from house dust mites (HDM), such as Dermatophagoides pteronyssinus (Der p) and Blomia tropicalis (Blo t), are central mediators of allergic sensitization and chronic inflammation. These TCRs, typically expressed on CD4+ T helper 2 (Th2) cells, recognize allergen peptides presented by Major Histocompatibility Complex (MHC) class II molecules, such as HLA-DRB1, on the surface of antigen-presenting cells (Source: UniProt; PubMed, PMID: 28434521). Upon binding, the TCR initiates a signaling cascade that leads to the production of pro-inflammatory cytokines (IL-4, IL-5, and IL-13), which promote B-cell isotype switching to IgE and the recruitment of eosinophils to the airways (Source: NIH, NIAID). In therapeutic contexts, these TCRs are the primary targets for allergen immunotherapy (AIT), which aims to modify the underlying disease by inducing immune tolerance. By repeatedly exposing the TCR to specific peptides, AIT promotes the expansion of regulatory T cells (Tregs) and reduces the Th2-mediated hypersensitivity response (Source: PubMed, PMID: 31600381). Understanding the specific TCR-peptide-MHC interaction for major allergens like Der p 1, Der p 2, and Blo t 5 is critical for the development of next-generation peptide-based vaccines and precision diagnostics for asthma and allergic rhinitis (Source: World Allergy Organization).

Other names

House dust mite-specific T-cell receptorDer p-specific TCRBlo t-specific TCRAntigen-specific T-cell receptorTCR recognizing Dermatophagoides pteronyssinus and Blomia tropicalis peptides

Allergen immunotherapy (AIT) targets these TCRs by providing repeated, controlled exposure to allergen-derived peptides. This process induces peripheral T-cell tolerance through mechanisms such as T-cell anergy, deletion, or the induction of regulatory T cells (Tregs) that secrete inhibitory cytokines like IL-10 and TGF-beta, effectively shifting the immune response from a Th2-driven allergic state to a Th1 or regulatory state (Source: PubMed, PMID: 30243711).