NKT cells provide help for dendritic cell-dependent priming of MHC class I-restricted CD8+ T cells in vivo.

Dendritic cells (DC) are potent APCs for naive T cells in vivo. This is evident by inducing T cell responses through adoptive DC transfer. Priming specific CTL responses in vivo often requires "help".

The immunodominant, Ld-restricted T cell response to hepatitis B surface antigen (HBsAg) efficiently suppresses T cell priming to multiple Dd-, Kd-, and Kb-restricted HBsAg epitopes.

MHC-I-restricted CTL responses of H-2(d) (L(d+) or L(d-)) and F(1) H-2(dxb) mice to hepatitis B surface Ag (HBsAg) are primed by either DNA vaccines or HBsAg particles. The D(d)/S(201-209) and K(d)/S(199-208) epitopes are generated by processing endogenous HBsAg; the K(b)/S(208-215) epitope is generated by processing exogenous HBsAg; and the L(d)/S(28-39) epitope is generated by exogenous as well as endogenous processing of HBsAg. DNA vaccination primed high numbers of CTL specific for the L(d)/S(28-39) HBsAg epitope, low numbers of CTL specific for the D(d)/S(201-209) or K(d)/S(199-208) HBsAg epitopes in BALB/c mice, and high numbers of D(d)/S(201-209)- and K(d)/S(199-208)-specific CTL in congenic H-2(d)/L(d-) dm2 mice.

Priming Th1 immunity to viral core particles is facilitated by trace amounts of RNA bound to its arginine-rich domain.

Particulate hepatitis B core Ag (C protein) (HBcAg) and soluble hepatitis B precore Ag (E protein) (HBeAg) of the hepatitis B virus share >70% of their amino acid sequence and most T and B cell-defined epitopes. When injected at low doses into mice, HBcAg particles prime Th1 immunity while HBeAg protein primes Th2 immunity. HBcAg contains 5-20 ng RNA/microg protein while nucleotide binding to HBeAg is not detectable.

Activating immunity in the liver. II. IFN-beta attenuates NK cell-dependent liver injury triggered by liver NKT cell activation.

Dendritic cell (DC)-dependent activation of liver NKT cells triggered by a single i.v. injection of a low dose (10-100 ng/mouse) of alpha-galactosyl ceramide (alphaGalCer) into mice induces liver injury.

Dendritic cells pulsed with exogenous hepatitis B surface antigen particles efficiently present epitopes to MHC class I-restricted cytotoxic T cells.

L(d)- and K(b)-binding epitopes processed by murine dendritic cells (DC) pulsed with exogenous, particulate hepatitis B surface antigen (HBsAg) are presented to cytotoxic T lymphocytes (CTL). The specific and dose-dependent induction of IFN-gamma release and cytotoxicity in CTL by metabolically active DC did not depend on antigenic peptides contaminating the particles, was cytochalasin D resistant, independent of the maturation state of DC, and blocked by primaquine, amiloride and NH(4)Cl (indicating involvement of acid proteolysis). The specific immunostimulatory phenotype of pulsed DC was maintained for about 3 h after the end of the pulse but rapidly decayed thereafter.