In attempt to increase the induction of peptide-specific cytolytic T c
ells (CTL) we investigated the effect of the Newcastle disease virus (
NDV) hemagglutinin-neuraminidase (HN) gene product on the activation o
f peptide-specific CTL. Spleen cells of CH3 mice immunized against the
influenza nucleoprotein peptide 50-63 (NP 50-63) were restimulated in
vitro (i) with peptide-pulsed syngeneic fibroblast cells (Ltk-) as an
tigen-presenting cells, which were in addition (ii) infected with NDV
or (iii) stably transfected with the HN cDNA of NDV. A greater than si
xfold increase in peptide-specific CTL responses was observed in cultu
res restimulated with peptide-pulsed Ltk- cells which coexpressed vira
l hemagglutinin due to either infection or transfection. A similar aug
mentation was seen in CTL responses against other types of antigen (ma
jor histocompatibility complex alloantigens, minor histocompatibility
antigens of tumor antigens) when suboptimal cultures were stimulated w
ith the respective antigen-presenting cells modified by NDV infection.
These findings suggest that NDV or viral HN expressed on antigen-pres
ent in cells or tumor cells can exert a T cell co-stimulatory function
.