CD4+ T-cell receptor recognizing influenza-derived peptides presented on MHC II (CD4+ TCR (Influenza/MHC II))

CD4+ T-cell receptors (TCRs) that recognize influenza-derived peptides presented on Major Histocompatibility Complex class II (MHC II) are central to the adaptive immune response against the influenza virus. These receptors, typically composed of alpha and beta chains, bind to specific viral epitopes—such as those derived from hemagglutinin (HA), neuraminidase (NA), or nucleoprotein (NP)—when they are displayed by antigen-presenting cells (Source: PubMed PMID: 30249038). Upon binding, the TCR triggers a signaling cascade that leads to the activation and differentiation of CD4+ T-cells into various effector subsets, including Th1 cells that secrete interferon-gamma and T follicular helper (Tfh) cells that provide essential help to B-cells for high-affinity antibody production (Source: NIH/NIAID). This interaction is crucial for both the clearance of primary infections and the establishment of long-term immunological memory. In the context of drug development, these TCRs are the primary targets for seasonal and universal influenza vaccines, which aim to expand the repertoire of influenza-specific CD4+ T-cells (Source: PubMed PMID: 28916533). Therapeutic strategies also explore the use of TCR-engineered T-cells or peptide-MHC complexes to modulate the immune response in severe cases or to improve vaccine efficacy across diverse HLA backgrounds.

Other names

Influenza-specific CD4+ T-cell receptorMHC class II-restricted influenza TCRHA-specific CD4+ TCRNP-specific CD4+ TCRT-cell receptor alpha/beta (Influenza-specific)

The TCR specifically recognizes and binds to influenza-derived peptides (e.g., from hemagglutinin or nucleoprotein) presented by MHC class II molecules on antigen-presenting cells. This binding event, stabilized by the CD4 co-receptor, initiates a signaling cascade through the CD3 complex and ZAP-70, leading to the activation of transcription factors like NFAT and NF-kappaB. This results in T-cell proliferation, differentiation into effector subsets (like Th1 or Tfh), and the secretion of cytokines that coordinate the broader immune response (Source: PubMed PMID: 25130604, 30249038).