Experiments designed to distinguish virus-specific from non-virus-specific
T cells show-ed that bystander T cells underwent apoptosis and substantial
attrition in the wake of a strong T-cell response. Memory CD8 T cells (CD8(
+) CD44(hi)) were most affected, During acute viral infection, transgenic T
cells that were clearly defined as non-virus specific decreased in number
and showed an increase in apoptosis. Also, use of lymphocytic choriomeningi
tis virus (LCMV) carrier mice, which lack LCMV-specific T cells, showed a s
ignificant decline in non-virus-specific memory CD8 T cells that correlated
to an increase in apoptosis in response to the proliferation of adoptively
transferred virus-specific T cells. Attrition of T cells early during infe
ction correlated with the alpha/beta interferon (IFN-alpha/beta) peak, and
the IFN inducer poly (I:C) caused apoptosis and attrition of CD8(+) CD44(hi
) T cells in normal mice but not in IFN-alpha/beta receptor-deficient mice.
Apoptotic attrition of bystander T cells may make room for the antigen-spe
cific expansion of T cells during infection and may, in part, account for t
he loss of T-cell memory that occurs when the host undergoes subsequent inf
ections.