T-cell receptor and B-cell receptor recognizing Enhanced Green Fluorescent Protein (EGFP) (TCR/BCR-EGFP)

Host adaptive immune receptors recognizing EGFP-derived peptides encompass the repertoire of T-cell receptors (TCRs) and B-cell receptors (BCRs) that specifically bind to epitopes derived from Enhanced Green Fluorescent Protein (EGFP). EGFP is a widely used reporter gene in biomedical research and gene therapy; however, because it is a non-mammalian protein derived from the jellyfish Aequorea victoria, it is frequently recognized as a foreign antigen by the host immune system (Stripecke et al., 1999, Gene Therapy). This recognition triggers an adaptive immune response, including the production of anti-EGFP antibodies and the activation of CD8+ cytotoxic T lymphocytes (CTLs) that can eliminate EGFP-expressing cells (Gambotto et al., 2000, Gene Therapy). In the context of gene therapy, these receptors represent a significant barrier, as they can lead to the rapid clearance of therapeutic vectors and the loss of transgene expression in both animal models and potentially human subjects (Ansari et al., 2016, Human Gene Therapy). Monitoring the activity of these receptors through ELISpot or ELISA is crucial for assessing the safety and longevity of EGFP-labeled cell therapies. While not a traditional therapeutic target for drug development, managing the activation of these receptors via transient immunosuppression is often essential for the success of experimental treatments involving fluorescent reporters.

Other names

Anti-EGFP immune receptorsEGFP-specific T-cell receptorsEGFP-specific B-cell receptorsAnti-GFP antibodiesHost immune response to EGFP

Recognition of EGFP-derived peptides presented on Major Histocompatibility Complex (MHC) molecules by T-cell receptors (TCRs), or direct recognition of the EGFP protein by B-cell receptors (BCRs), leading to the activation of cytotoxic T lymphocytes and the production of neutralizing antibodies. Immunosuppressive drugs act by inhibiting T-cell activation (calcineurin inhibitors) or broadly suppressing inflammatory cytokine production (corticosteroids) to prevent the clearance of EGFP-expressing cells.