ICAM-1 IS REQUIRED FOR T-CELL PROLIFERATION BUT NOT FOR ANERGY OR APOPTOSIS INDUCED BY STAPHYLOCOCCUS-AUREUS ENTEROTOXIN-B IN-VIVO

The response of T lymphocytes to superantigens requires expression of the appropriate TCR V-beta gene products as well as the establishment of cellular interactions mediated by adhesion molecules. To study the role of intercellular adhesion molecule (ICAM)-1 in the response in vi vo to superantigens, we have analyzed the effects induced by the bacte rial superantigen Staphylococcus aureus enterotoxin B (SEB) in mice wh ich have been made genetically deficient in ICAM-1. SEB treatment of w ild-type mice causes proliferation, deletion and anergy of the SEB-rea ctive V(beta)8(+) T cell population. Here we show that cellular intera ctions mediated by ICAM-1 are not essential for the induction of anerg y or for the deletion of CD4(+)V(beta)8(+) or CD8(+)V(beta)8(+) T cell s, but are required for the proliferation of these peripheral T lympho cytes. This is the first demonstration in vivo that the absence of the co-stimulatory signals provided by the interaction of ICAM-1 with its specific ligands impairs the proliferation of SEB-reactive T cells. I nterestingly, our study showed that SEB-induced proliferation of CD8()V(beta)8(+) T cells from lymph nodes (not from spleen) is independent of the interactions mediated by ICAM-1.