Inability of Viral Superantigens to Induce CD4-mediated Islet Transplant Rejection
Superantigens have the ability to bypass the specific interactions of the MHC class II and T-cell receptor by binding outside of the peptide binding region and onto the Vβ chain. This ability allows superantigens to stimulate a wide array of T-cell populations, irrespective of T-cell receptor (TCR) specificity. Research on bacterial and viral superantigens have demonstrated various outcomes ranging from superantigen dependent cellular cytoxicity (SDCC), rheumatoid arthritis, to superantigen stimulated T-cell clonal deletion and anergy. Due to its ability to proliferate a large population of T-cells, this paper asks whether superantigens have a role in islet transplant rejection. We used transgenic Vβ6 TCR mice specific for male ‘H-Y’ antigen as recipients to islet transplants. Donors comprised mice expressing endogenous superantigen specific for the Vβ6 chain. Transplantation of these donor islets did not induce rejection. Recipients were also primed with ‘H-Y’ antigen to induce a CD4 effector memory T-cell population prior to islet transplantation. Even with primed recipients, donor islet transplants did not induce rejection by recipient transgenic mice.