title: Accessory cell function of a human colonic epithelial cell line HT-29 for bacterial superantigens.
abstract: 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.
authors.affiliation: Third Department of Internal Medicine, Tohoku University School of Medicine, Aoba-ku, Sendai, Japan.
authors.forename: Z X
authors.initials: ZX
authors.lastname: Liu
authors.forename: S
authors.initials: S
authors.lastname: Sugawara
authors.forename: N
authors.initials: N
authors.lastname: Hiwatashi
authors.forename: M
authors.initials: M
authors.lastname: Noguchi
authors.forename: H
authors.initials: H
authors.lastname: Rikiishi
authors.forename: K
authors.initials: K
authors.lastname: Kumagai
authors.forename: T
authors.initials: T
authors.lastname: Toyota
mesh_terms: D000938:Antigen-Presenting Cells / Q000502:physiology*; D004768:Enterotoxins / Q000276:immunology*; D006684:HLA-DR Antigens / Q000502:physiology; D019073:HT29 Cells; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000502:physiology; D016209:Interleukin-8 / Q000096:biosynthesis; D007422:Intestines / Q000276:immunology*; D008213:Lymphocyte Activation; D018089:Superantigens / Q000276:immunology*
chemical_list: D004768:Enterotoxins; D006684:HLA-DR Antigens; D016209:Interleukin-8; D018089:Superantigens; D018799:Intercellular Adhesion Molecule-1; C031818:enterotoxin B, staphylococcal