Open AccessInvolvement of HLA class II molecules in acquisition of staphylococcal enterotoxin A‐binding activity and accessory cell activity in activation of human T cells by related toxins in vascular endothelial cells
Author(s) -
UCHIYAMA T.,
ARAAKE M.,
YAN X. J.,
MIYANAGA Y.,
IGARASHI H.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb02995.x
Subject(s) - enterotoxin , interferon gamma , human leukocyte antigen , stimulation , biology , microbiology and biotechnology , t cell , mhc class ii , hla dr , endothelial stem cell , immunology , cytokine , antigen , immune system , in vitro , biochemistry , endocrinology , gene , escherichia coli
SUMMARY Human umbilical vascular endothelial cells (HUVEC) express HLA class II molecules upon stimulation with recombinant human interferon‐gamma (IFN‐γ). Staphylococcal enterotoxin (SE) A (SEA)‐binding assay using [ 125 I]‐SEA showed the presence of specific SEA binding in HUVEC stimulated with IFN‐γ but not in unstimulated HUVEC. Levels of HLA class II expression and SEA‐binding increased as the IFN‐γ concentration and the period of stimulation were increased. Binding of [1 254 I]‐SEA to the IFN‐γ‐stimulated HUVEC was reduced markedly by an anti‐DR/DP MoAb. T cells produced IL‐2 upon stimulation with a group of SEs (SEA, SEB, SEC, SED and SEE) in the presence HUVEC stimulated with IFN‐γ but not in the presence of control HUVEC. The level of accessory cell activity in the IFN‐γ‐stimulated HUVEC was related to the level of HLA class II expression and SEA‐binding activity. Antibodies to HLA class II molecules almost completely inhibited the response. These results indicate that HLA class II molecules are directly involved in the acquisition of these activities in HUVEC.