A macaque model was employed to explore staphylococcal enterotoxin B (
SEB) superantigen-driven T lymphocyte responses. The SEE-reactive V be
ta(+) cell subpopulations demonstrated a striking tri-phase response i
n rhesus monkeys following an SEE challenge in vivo. The hyperacute do
wn-regulation, seen as early as 2 h through 2 days after SEE injection
, was characterized by a disappearance of the reactive V beta-restrict
ed PBL subpopulations from the circulation and decreased expression of
these cell subpopulations in lymphoid tissues. Following this, a domi
nant expansion of reactive V beta-expressing CD4(+) cell subpopulation
s occurred in lymph nodes and spleens, whereas in the peripheral blood
a preferential expansion of reactive V beta-expressing CD8(+) cell su
bpopulations was seen. An exhaustion of this response was then seen, w
ith a prolonged decrease in the number of the reactive V beta(+) CD4() lymphocyte subpopulations. Interestingly, monoclonal or oligoclonal
dominance was seen in the reactive V beta(+) cell subpopulations in th
e period of the transition from the polyclonal cellular expansion to t
he exhaustion of the response, suggesting that some V beta(+) cell. cl
ones may be more resistant than others to superantigen-mediated deplet
ion. These results indicate that in vivo SEE superantigen-mediated eff
ect on lymphocyte subpopulations in macaques is complex, suggesting th
at profound dynamics in the TCR repertoires may in part account for th
e susceptibility of higher primates to SEE-induced diseases.