Effect of immunoglobulin G from patients with Graves’ ophthalmopathy and in terferon gamma in intercellular adhesion molecule-1 and human leucocyte antigen-DR expression in human retroocular fibroblasts

Objective To detect the expression of intercellular adhesion molecule-1 (ICAM-1) and human leucocyte antigen-DR (HLA-DR) on retroocular fibroblasts (RFs) by immunoglobulin G (IgG) from patients with Graves’ ophthalmopathy (GO) and interferon gamma (IFN-γ) and to study the possible mechanism of humoral immunity and cellular immunity in the pathogenesis of GO. Methods Purified IgG was obtained from 23 patients (GO 10, Graves’ disease 9, toxic multinodular goiter 4) and 8 normal persons. Cytokine IFN-γ and thyroid stimulating hormon (TSH) were incubated with normal human RF cultured in vitro. Antigen expression on RFs induced by stimulators was examined using immunofluoresence staining and a flow cytometer. Results RFs spontaneously expressed ICAM-1, but did not express HLA-DR. All IgGs from patients with GO and other thyroid diseases as well as from normal persons could not stimulate the expression of ICAM-1 on RFs. IFN-γ and TSH significantly enhanced the expression of ICAM-1 in dose-dependent manner (P<0.05). Only IFN-γ could stimulate RFs to express HLA-DR (P<0.05). Conclusions IgG from patients with GO did not stimulate the expression of ICAM-1 and HLA-DR on the surface of cultured normal human RFs. IFN-γ was the important factor for initiating and promoting autoimmune reactions in GO. We need to pay more attention to TSH, as it may possibly play a promoting role in the pathogenesis in GO.

Effect of immunoglobulin G from patients with Graves' ophthalmopathy and interferon gamma in intercellular adhesion molecule-1 and human leucocyte antigen-DR expression in human retroocular fibroblasts

OBJECTIVE: To detect the expression of intercellular adhesion molecule-1 (ICAM-1) and human leucocyte antigen-DR (HLA-DR) on retroocular fibroblasts (RFs) by immunoglobulin G (IgG) from patients with Graves' ophthalmopathy (GO) and interferon gamma (IFN-gamma) and to study the possible mechanism of humoral immunity and cellular immunity in the pathogenesis of GO. METHODS: Purified IgG was obtained from 23 patients (GO 10, Graves' disease 9, toxic multinodular goiter 4) and 8 normal persons. Cytokine IFN-gamma and thyroid stimulating hormone (TSH) were incubated with normal human RF cultured in vitro. Antigen expression on RFs induced by stimulators was examined using immunofluoresence staining and a flow cytometer. RESULTS: RFs spontaneously expressed ICAM-1, but did not express HLA-DR. All IgGs from patients with GO and other thyroid diseases as well as from normal persons could not stimulate the expression of ICAM-1 on RFs. IFN-gamma and TSH significantly enhanced the expression of ICAM-1 in dose-dependent manner (P < 0.05). Only IFN-gamma could stimulate RFs to express HLA-DR (P < 0.05). CONCLUSIONS: IgG from patients with GO did not stimulate the expression of ICAM-1 and HLA-DR on the surface of cultured normal human RFs. IFN-gamma was the important factor for intiating and promoting autoimmune reactions in GO. We need to pay more attention to TSH, as it may possibly play a promoting role in the pathogenesis in GO.