TCR V-beta usage was examined in C57BL/6 mice infected with Plasmodium
yoelii. In addition to a polyclonal T cell activation, already descri
bed, a superantigenic-like activity was observed during the acute infe
ction, This superantigenic activity induces a preferential deletion wi
thout prior expansion of CD4(+) and CD8(+) T cells bearing the TCR V(b
eta)9 segment. The superantigen could be released by the parasite at d
ifferent stages of its development since the deletion of V(beta)9(+) T
cells was observed in blood and lymph nodes of mice infected either w
ith sporozoites or with erythrocytic stages, Injection of sporozoite o
r parasitized erythrocytes to newborn mice led to a deletion and anerg
y of peripheral V(beta)9(+) T cells, without affecting thymic T cell p
opulations, These observations suggest that the superantigen is releas
ed at very low concentrations during parasite development. The role of
such parasite superantigenic activity in infectivity can be underline
d by the observation that congenic BALB.D2 Mls1(a) mice lacking V(beta
)9 T cells are more susceptible to infection by P. yoelii.