Chinese medical journal · 2000
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.
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Li Y, Chen L, Teng W, Shan Z, Li Z
Аннотация
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.
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.