CD154:CD11b blockade increases MPEC differentiation of virus-specific CD8 +T cells

Abstract CD154 pathway blockade has been shown to significantly improve graft survival in transplantation. Recently, CD11b was identified as an alternate receptor for CD154. CD154:CD11b interactions promote rejection by increasing the recruitment of innate and adaptive immune cells into allograft. However, effects on protective response infection during immunosuppression not elucidated. To address this, MHV68, a murine homolog EBV, used assess antigen-specific CD8 +T cell response. Naïve B6 mice were infected with MHV68 treated days 0, 2, 4, 6 peptide inhibitor binding (cM7). cM7 treatment resulted increase tetramer +antigen-specific 10 post-infection that exhibited gene expression associated activation antigen processing. determine if this result enhanced proliferation, CTV-labeled OT-I T stimulated vitro presence or absence blockade. Results indicated did impact proliferation. Instead, CD69, CD25, CD44, vivo CD127 hiKLRG1 loMPECs. In conclusion, these data demonstrate enhances quantity quality virus-specific immunity. We speculate could be due inhibition terminal differentiation resulting high memory precursors, altered balance CD154:CD40 vs binding, CD40-driven costimulation. Supported grants from NIH (R01 AI152516)