It is now well established that viral infections can induce large expansion
s of Ag-specific CD8(+) T cells. These cells divide very rapidly with an es
timated doubling time of similar to6 h. When virus is cleared, the vast maj
ority of these effector CD8 T cells undergo apoptosis. The remaining memory
cells persist at constant levels and provide the basis for the accelerated
recall response upon rechallenge. The molecular mechanisms that control th
e rapid proliferation and death of Ag-specific T cells are poorly understoo
d. Because of its important role in controlling cell proliferation and deat
h, we examined antiviral immune responses in p53(-/-) mice using lymphocyti
c choriomeningitis virus. We found that effector CD8 and CD4 responses were
comparable but that memory levels were slightly higher in -/- mice compare
d with +/+ mice. The lack of a major difference in virus-specific T cell re
sponses between +/+ and -/- mice suggests that p53 only plays a minor role
in regulating the proliferation, apoptosis, and maintenance of Ag-specific
T cells. Thus, it appears that the primary function of p53 is in controllin
g "illegitimate" proliferation and tumor development and not in regulating
Ag-specific T cell responses.