MHC GENOTYPE CONTROLS THE CAPACITY OF LIGAND DENSITY TO SWITCH T-HELPER (TH)-1 TH-2 PRIMING IN-VIVO/

A quantitative mechanism for the differentiation of CD4 T cells into r ecognized subsets of Th1 and Th2 effecters is controversial. Here, we define the Ag dose more precisely to the density of a minimal immunoge nic peptide presented on the surface of a specific APC type, Th1 and T h2 responder MHC genotypes differ by as much as an order of magnitude in the density of this peptide displayed on B7-2(+) B cells. We asked whether such B cells presenting a low ligand density primed Th2 effect ers in an MHC genotype with predisposed high-density presentation and Th1-type immunity, and whether high ligand density B cells primed Th1 effecters in an MHC genotype that normally presents a low density and the Th2 phenotype. While low ligand density had the capacity to switch phenotype in the Th1 responder, high-density presentation did not alt er genetically determined Th2 responder status.