House dust mite-specific T-cell receptor (HDM-specific TCR) (HDM-specific TCR)

House dust mite-specific T-cell receptors (HDM-specific TCRs) are specialized antigen-recognition complexes expressed on the surface of T-lymphocytes, particularly CD4+ T-helper cells. These receptors specifically bind to peptides derived from house dust mite (HDM) allergens, such as Der p 1, Der p 2, and Der p 23, when they are presented by Major Histocompatibility Complex (MHC) class II molecules on antigen-presenting cells (Wambre et al., 2012, J Allergy Clin Immunol). This recognition event is a critical checkpoint in the development of allergic diseases, including allergic asthma and rhinitis, as it triggers the activation and expansion of Th2 cells that drive IgE-mediated hypersensitivity (Gafvelin et al., 2007, Int Arch Allergy Immunol). In therapeutic contexts, HDM-specific TCRs are the primary targets of allergen-specific immunotherapy (AIT), such as Acarizax or Odactra, which aim to induce immune tolerance through mechanisms like T-cell anergy or the induction of regulatory T-cells (Tregs) (Akdis & Akdis, 2014, J Allergy Clin Immunol). Research into the TCR repertoire of HDM-allergic patients has revealed specific motifs and gene usage patterns that could serve as biomarkers for disease severity or treatment response (Seumois et al., 2016, Nat Commun). Furthermore, novel strategies are exploring the use of TCR-engineered T-cells or peptide-based vaccines to precisely modulate the immune response directed at these receptors (Larché, 2007, Nat Rev Immunol).

Other names

Dermatophagoides-specific T-cell receptorHDM-reactive TCRDer p-specific T-cell receptorDer f-specific T-cell receptorHDM-specific T-cell receptor recognizing HDM peptide-MHC class II complexes

Allergen-specific immunotherapy (AIT) targets HDM-specific TCRs by providing chronic, low-dose antigen exposure, which shifts the T-cell response from a pro-allergic Th2 phenotype to a tolerant state characterized by the production of IL-10 and TGF-beta by regulatory T-cells (Tregs) and the induction of IgG4 blocking antibodies (Akdis & Akdis, 2014, J Allergy Clin Immunol).