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* Howard Hughes Medical Institute, Departments of Microbiology and Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75235
Most CTL responses to epitopes from influenza virus are restricted
by MHC class Ia molecules. However, a synthetic peptide corresponding
to residues 173 to 190 of influenza A/JAP/305/57 hemagglutinin (HA) can
induce, in vitro, a CTL response to peptide presented by a mouse class
Ib molecule encoded by a gene telomeric to H2-Q. Here, we
identify the molecule as H2-M3 and show that the last five residues of
HA173–190, MLIIW, is the minimal epitope for CTL recognition. Cells
that express M3wt, from C57BL/6 or BALB/c mice, are
sensitized by both MLIIW and the longer peptide HA173–190, whereas
cells that express M3f, from A.CA or B10.M mice, are
sensitized only by MLIIW; a single amino acid change at residue 31
(V
M) of M3 accounts for this difference. Although M3-restricted CTLs
preferably recognize N-formylated epitopes, i.e., those of
mitochondrial or prokaryotic origin, our findings show that
M3-restricted primary CTL responses can be generated in vitro against
nonformylated epitopes.
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