Open AccessSynovial cells are potent antigen‐presenting cells for superantigen, staphylococcal enterotoxin B (SEB)
Author(s) -
ORIGUCHI T.,
EGUCHI K.,
KAWABE Y.,
MIZOKAMI A.,
IDA H.,
NAGATAKI S.
Publication year - 1995
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.1365-2249.1995.tb05556.x
Subject(s) - superantigen , enterotoxin , immunology , microbiology and biotechnology , antigen , staphylococcus aureus , antigen presenting cell , biology , medicine , t cell , immune system , bacteria , escherichia coli , gene , genetics , biochemistry
SUMMARY There is ample evidence suggesting that superantigens may act as a triggering factor in the pathogenesis of rheumatoid arthritis (RA). We investigated whether superantigen could activate T cells in the presence of synovial cells. T cells were cultured with SEB in the presence of interferongamma (IFN‐γ)‐treated synovial cells. T cell proliferation and activation were assessed by 3 H‐thymidine incorporation and IL‐2 production. The expression of HLA class II antigens and adhesion molecules on synovial ceils was detected by flow cytometer. In the presence of IFN‐γ‐treated synovial cells, T cells proliferated vigorously and produced IL‐2 in response to SEB. A low SEB‐induced T cell response was noticed in the presence of untreated synovial cells. Allogeneic as well as autologous IFN‐γ‐treated synovial cells markedly enhanced SEB‐induced T cell proliferation. IFN‐γ‐treated synovial cells had increased expression of HLA class II antigens and intercellular adhesion molecule‐1 (ICAM‐1) adhesion molecules. MoAbs towards these antigens markedly inhibited the SEB‐induced T cell response. These results indicate that activated synovial cells are potent antigen‐presenting cells for SEB to T cells, and that superantigens may play a critical role in the pathogenesis of RA through activated synovial cells.