VIRAL PEPTIDE-SPECIFIC INDUCTION OF MHC CLASS-II EXPRESSION BY MURINET-CELL CLONES

We report that I-A(b)-restricted T cell clones, elicited by influenza infection of C57BL/10 mice and specific for the hemagglutinin peptide HA1 186-205, express class II, They respond to peptide stimulation by IL release (IL-3 or IFN-gamma) without a requirement for APC hut do no t proliferate, Moreover, surface expression of class II requires de no vo synthesis in the presence of the stimulatory peptide and is inhibit ed by coculture with TCR-specific Ab, or brefeldin A or cycloheximide, Clonotypic specificity of peptide induction was confirmed by failure of other allele specific peptides to enhance class II expression. Addi tion of the viral peptide to T cells induced homotypic adhesion, which provides a physical basis for stabilization of class II-peptide compl exes at the cell surface, Extinction of class II expression was eviden t in the corresponding T cell hybridomas, which might account for the failure to report class II expression by murine T cells, Control studi es indicated that class II was not passively acquired from APC by demo nstrating 1) failure of processed Ag to induce class II expression, 2) allo-class II (A(k)) was not acquired by coculture with peptide and s emisyngeneic (H-2(b/k)) APC, 3) absence of class It expression by a NP peptide-specific Th2 clone under identical culture conditions, and mo st significantly, 4) reverse-transcriptase PCR amplification and surfa ce expression of class ii using highly purified preparations of FACS-s elected CD4(+) class II- cells cocultured with the stimulatory peptide .