Induction of T cell tolerance by pretreatment with anti-ICAM-1 and anti-lymphocyte function-associated antigen-1 antibodies prevents antigen-induced eosinophil recruitment into the mouse airways.

To determine whether the induction of Th2 cell tolerance down-regulates Ag-induced eosinophil recruitment into the tissue, we studied the effect of the in vivo pretreatment with anti-ICAM-1 mAb, anti-LFA-1 mAb, and a soluble Ag on Ag-induced eosinophil infiltration in the trachea of sensitized mice. The in vivo pretreatment with anti-ICAM-1 mAb, anti-LFA-1 mAb, and a soluble Ag inhibited Ag-induced eosinophil infiltration in the mouse trachea in an Ag-specific manner. The pretreatment with anti-LFA-1 mAb and the Ag also had a weak inhibitory effect on the Ag-induced eosinophil infiltration. In contrast, the pretreatment with Ag alone, the combination of anti-ICAM-1 mAb and anti-LFA-1 mAb alone, or the combination of anti-ICAM-1 mAb and the Ag had no significant effect. In addition, the pretreatment with the two mAb and the Ag and, to a lesser degree, the pretreatment with anti-LFA-1 mAb and the Ag also prevented Ag-specific IgE production in mice. In vitro Ag-induced IL-2, IL-4, and IL-5 production was decreased in spleen cells of the mice pretreated with anti-ICAM-1 mAb, anti-LFA-1 mAb, and the Ag, but not with Ag alone or with the combination of anti-ICAM-1 mAb and anti-LFA-1 mAb alone, indicating the induction of both Th1 and Th2 cell tolerance in vivo. These results indicate that the induction of Th2 cell tolerance prevents Ag-induced eosinophil recruitment into the tissue and IgE Ab production and that ICAM-1/LFA-1 interaction is involved as a costimulatory signal in inducing T cell tolerance to a soluble Ag.