Accessory cell function of a human colonic epithelial cell line HT‐29 for bacterial superantigens
The expression and up‐regulation of cell adhesion molecules on a human colonic epithelial cell line HT‐29, and the peripheral blood T lymphocyte proliferation responses to bacterial superantigens presented by this cell line were investigated, compared with peripheral blood monocytes. In HT‐29 cells, there was constitutive expression of intercellular adhesion molecule‐1 (ICAM‐1) and lymphocyte function‐associated antigen‐3 (LFA‐3) at a low level, but no constitutive expression of HLA‐DR, LFA‐1, B7‐1 and B7‐2 molecules. After stimulation with the supernatants of staphylococcal enterotoxin B (SEB)‐stimulated peripheral blood mononuclear cells for 48 h, there was significant up‐regulation of HLA‐DR and ICAM‐1 molecules (both >90% positive). However, this stimulation had no effect on the expression of LFA‐1, B7‐1, B7‐2 and LFA‐3 molecules. In the presence of all tested superantigens SEB, toxic shock syndrome toxin‐1, and streptococcal pyogenic exotoxin A, stimulated HT‐29 cells caused significant T cell proliferation. When monocytes were used as antigen‐presenting cells (APC), the MoAbs against HLA‐DR, B7‐2 and LFA‐3 showed a significant inhibition of SEB‐induced T cell proliferation. Anti‐ICAM‐1 MoAb had no effect on this response. On the other hand, when stimulated HT‐29 cells were used as APC, the MoAbs against HLA‐DR and ICAM‐1 significantly inhibited SEB‐induced T cell proliferation. In contrast to monocytes, anti‐B7‐2 and anti‐LFA‐3 had no effect on this response. SEB could not induce HT‐29 cells to produce IL‐8 directly; however, SEB significantly induced the stimulated HT‐29 cells to produce IL‐8 in the presence of T cells. Thus these data demonstrate that the products of superantigen‐stimulated T cell activation can increase the expression of HLA‐DR and ICAM‐1 molecules on HT‐29 cells significantly. Stimulated HT‐29 cells can serve as APC to bacterial superantigens. This response is an HLA‐DR‐ and ICAM‐1‐dependent, but B7‐2‐ and LFA‐3‐independent process, which was different from professional APC monocytes.