66 HUMAN INTRAVENOUS GAMMAGLOBULIN (HIVIG) REOUCES THE IN VITRO CYTOTOXIC ACTIVITY OF KAWASAKI SYNDROME (KS) SERA ON INTERLEUKIN (IL-1|[alpha]|) TREATED CULTURED HUMAN UMBILICAL VEIN ENDOTHELIUM (HUVE)

Sera from patients with acute KS cause complement-mediated lysis of IL-1α stimulated HUVE (D.Y.M. Leunn et al. I. Exp. Med. 164. 1950-72, 1986). In vitro cultured HUVE monolayers were labelled with 51Cr and treated with hu rIL-1α(10 U/ml) for 4 hours. Addition of KS sera (1:2.5) to the culture caused a 28.6±7.3% (n=7) 51Cr release in the presence of complement. The addition of HIVIG (Gamma immune 0.5%) to the culture reduced the HUVE lysis tD 12.3±5.2%. Sera from patients in the convalescent phase of KS (n=4) had no cytotoxic effect. We conclude that cytotoxic antibodies in acute KS sera directed to IL-1α inducible endothelial cell antigens may compete for receptor sites with antibodies present in HIVIG preparations that fail to fix complement. This competition may result in the decrease of the cytotoxicity by KS sera and in consequence in the beneficial effect of HIVIG in KS.