Monocyte inflammatory protein-1 alpha facilitates priming of CD8(+) T cellresponses to exogenous viral antigen

Dendritic cells (DC) derived from bone marrow precursors of BALB/c or C57BL /6 mice in low-serum cultures supplemented with granulocyte macrophage colo ny stimulating factor and Fits ligand were pulsed in vitro with hepatitis B surface antigen (HBsAg) particles, DC processed exogenous HBsAg and presen ted its MHC class I-binding epitopes to cytotoxic T lymphocytes (CTL). This specific and restricted interaction of DC with CTL stimulated release of I FN-gamma and macrophage inflammatory protein (MIP)-1 alpha from the respond ing CTL, MIP-1 alpha enhanced the survival of DC in vitro but did not induc e proliferation, Furthermore, co-delivery of MIP-1 alpha facilitated CTL pr iming in vivo to exogenous HBsAg in low responder C57BL/6 (H-2(b)) mice: a single injection of a low dose of HBsAg particles (without further adjuvant s) successfully primed K-b-restricted CTL responses to HBsAg only when the exogenous antigen was co-delivered with 100 ng MIP-1 alpha. These in vitro and In vivo data point to an important role of MIP-1 alpha in the DC-depend ent priming of CTL to exogenous viral antigens.