(A) 345-360 365-380 1968 DLRVLSFIRGTKVSPRGKLSTRGVQIASNENMDAMESSTLELRS 1934 DLRVLSFIKGTKVVPRGKLSTRGVQIASNENMETMESSTLELRS 369-382 (B) 1968 1934 80 60 40 20 none 1968 1934 345- 365- 369- 365- 369- strain strain 360 380 382 380 382 Figure Q24-1 Viral nuclear protein recognition by cytotoxic T cells (Problem 24-7). (A) Sequences of a segment of the nuclear protein from the 1968 and 1934 strains of influenza virus. Peptides used in the experiments in (B) are highlighted by pink bars. The amino acid differences between the viral proteins are highlighted in blue. (B) Cytotoxic T-cell-mediated lysis of target cells. The target cells were untreated (none), infected with virus (1968 or 1934 strain), or preincubated with high concentrations of the indicated viral peptide. cell lysis
For many years it was a complete mystery how
cytotoxic T cells could see a viral protein that seemed to be
present only in the nucleus of the virus-infected cell. The
answer was revealed in a classic paper that took advan-
tage of a clone of T cells whose T cell receptor was directed
against an antigen assoicated with the nuclear protein of
the 1968 strain of influenza virus. The authors of the paper
found that when they incubated high concentrations of
certain peptides derived from the viral nuclear protein, the
cells became sensitive to lysis by subsequent incubation
with the cytotoxic T cells. Using various peptides from the
1968 strain and the 1934 strain (with which the cytotoxic T
cells did not react), the authors defined the particular pep-
tide responsible for the T cell response (Figure Q24–1).
A. Which part of the viral protein gives rise to the
peptide that is recognized by the clone of cytotoxic T cells? Why do not all viral peptides sensitize the target cells for
lysis by the cytotoxic T cells?
B. It is thought the MHC molecules come to the cell
surface with peptides already bound. If that is so, how do
you imagine that these experiments worked?
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