E‐selectin is an endothelial adhesion molecule for polymorphonuclear cells, monocytes and skin‐homing T cells. We have analyzed whether murine T cells are able to induce expression of E‐selectin in vitro and in vivo. Using models of inflammation in which T cells play either a significant or only a minor role, we compared induction of E‐selectin between normal mice and mice lacking functional T cells (athymic nude mice). In irritant contact dermatitis, a model without a major role for T cells, E‐selectin was transiently expressed within the first 24 h in both normal and nude mice. In experimental leishmaniasis (where specific T cells play an important role), a high expression of E‐selectin was maintained for 48 h in normal mice, whereas in nude mice expression was only transient. However, reconstitution of nude mice with 10⁸ T cells from draining lymph nodes (LN) of Leishmania‐infected normal mice could restore sustained expression of E‐selectin. Transfer of T lymphocytes from normal LN or from LN of mice sensitized to the contact allergen trinitrochlorbenzene (TNCB) did not have this effect. T cells from TNCB‐sensitized mice, however, did induce sustained expression of E‐selectin in nude mice when TNCB was applied locally; here, reconstitution with Leishmania‐specific T cells had no effect. In vitro, T cells from infected or TNCB‐sensitized normal mice increased expression of E‐selectin on microvascular endothelial cells after 4 h of co‐culture. T cells from untreated mice were less effective. Induction was dependent on direct cell‐cell contact, but not on the action of interleukin‐1α, interleukin‐1β, tumor necrosis factor‐α or interferon‐γ. We conclude that sensitized T cells induce sustained expression of E‐selectin in vivo in an antigen‐dependent manner. This novel way of regulation could be relevant for cell‐mediated immunity and chronic disease. The mechanisms are unknown, but, as in vitro, might require direct cell‐cell contact.