Most of the data accumulated to date on the immunoregulatory effects of pro
staglandins (PG) on T cell activation stem from the archetypal inhibitory e
ffect of PGE(2). In this study we provide instead, the first evidence that
exogenous PGB(2), a catabolic metabolite of PGE(2), synergizes with signals
delivered by T cell receptor (TCR) engagement to induce interleukin-2 (IL-
2) production and IL-2 receptor (IL-2R) alpha-expression in Jurkat cells. A
ccordingly, PGB(2) enhances the proliferation of anti-CD3-activated periphe
ral blood lymphocytes (PBL), In terms of cellular signaling, we present evi
dence that PGB(2) activates tyrosine kinase activities and efficiently incr
eases c-fos mRNA expression and nuclear factor-kappa B (NF-kappa B) translo
cation to the nucleus. Owing to these features, PGB(2) appears as a new lip
id mediator capable of delivering an ancillary signal leading to T lymphocy
te activation.