T-cell receptor specific for CRM197-derived peptides bound to HLA class II (CRM197-specific TCR)

T-cell receptors (TCRs) specific for CRM197-derived peptides bound to HLA class II molecules are specialized immune sensors that recognize the cross-reacting material 197 (CRM197), a non-toxic mutant of the diphtheria toxin. CRM197 is extensively utilized as a carrier protein in conjugate vaccines to enhance the immunogenicity of polysaccharide antigens by recruiting T-cell help (Broker et al., 2011). These TCRs are primarily expressed on CD4+ T lymphocytes and are responsible for identifying specific CRM197 peptide fragments presented by Human Leukocyte Antigen (HLA) class II molecules on antigen-presenting cells (Avci et al., 2011). Upon recognition, the TCR initiates a signaling cascade that leads to T-cell activation, cytokine production, and the subsequent stimulation of B cells to produce high-affinity antibodies. This mechanism is fundamental to the efficacy of widely used vaccines against pathogens such as Streptococcus pneumoniae and Neisseria meningitidis (Paliard et al., 2000). Beyond vaccine science, these TCRs are being investigated in the context of TCR-engineered T-cell therapies and as tools for monitoring immune repertoire diversity (Repertoire Immune Medicines, 2023). Understanding the specificity and HLA-restriction of these TCRs is crucial for predicting vaccine responsiveness across diverse populations.

Other names

CRM197-specific T-cell receptorCD4+ T-cell receptor for CRM197Diphtheria toxin mutant CRM197-specific TCRCRM197-reactive TCR

The T-cell receptor (TCR) recognizes and binds to specific CRM197-derived peptides presented by HLA class II molecules on the surface of antigen-presenting cells. This binding event, in the presence of co-stimulatory signals, triggers a signal transduction cascade through the CD3 complex, leading to T-cell activation, proliferation, and the secretion of cytokines that facilitate B-cell maturation and antibody class switching (Avci et al., 2011; Broker et al., 2011).