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ICAM‐1 costimulation induces IL‐2 but inhibits IL‐10 production in superantigen‐activated human CD4+ T cells

We have previously reported that costimulatory pathways including B7–CD28 and lymphocyte function‐associated antigen‐3 (LFA‐3)–CD2 shape distinct activation profiles in human CD4+ T cells. We now show that superantigen (SAg), in combination with intracellular adhesion molecule‐1 (ICAM‐1) costimulation drives a proliferative response accompanied by high levels of interleukin‐2 (IL‐2) and moderate levels of interferon‐γ (IFN‐γ) and tumour necrosis factor (TNF). This response profile differs from that observed in B7 or LFA‐3 costimulated T cells because our previous results showed that B7–CD28 costimulation was accompanied by high levels of IL‐2, IFN‐γ and TNF, whereas LFA‐3 was a potent inducer of IFN‐γ and TNF, but had little influence on IL‐2 production. The ICAM‐1‐induced IL‐2 production could efficiently be abrogated with monoclonal antibody (mAb) against ICAM‐1 or LFA‐1, showing that the activation is dependent of a functional ICAM‐1–LFA‐1 pathway. SAg‐induced IL‐2, IFN‐γ and TNF were detected in both CD4+ and CD8+ T cells, whereas production of IL‐10 was restricted to CD4+ T cells. A major finding in the present study was that ICAM‐1 costimulation strongly inhibits IL‐10 production in CD4+ T cells. Our data demonstrate that ICAM‐1 costimulation is sufficient to induce large amounts of IL‐2. The presence of ICAM‐1 results in suppression of IL‐10 production in T helper (Th) cells, which may favour the development of Th1 and not Th2 T cells.