Sakaguchi Kohsaku, Kitano Motoko, Nishimura Mamoru, Senoh Tomonori, Ohta Takeyuki, Terao Masako, Shinji Noriyuki, Koide Norio, Tsuji Takao
First Department of Internal Medicine, Okayama University Medical School, Okayama, Japan.
Hepatogastroenterology. 2004 Nov-Dec;51(60):1780-3.
BACKGROUND/AIMS: To evaluate the association of the immunosuppressive effects of transforming growth factor-beta1 (TGF-beta1) with abnormalities in immune regulation in autoimmune hepatitis (AIH), we investigated the serum level of TGF-beta1 and expression of TGF-beta receptor type II (TbetaRII) in peripheral blood mononuclear cells (PBMC) in patients with AIH.
Twenty-two patients with AIH were included in this study. Serum levels of total TGF-beta1 were determined using a specific enzyme-linked immunosorbent assay (ELISA). The expression levels of TbetaRII mRNA were semi-quantitatively determined by ribonuclease (RNase) protection assay specific for TbetaRII.
The mean serum level of TGF-beta1 in patients with AIH (230+/-95 ng/mL) was higher than that of healthy controls (137+/-81 ng/mL, p=0.012). The expression level of TbetaRII mRNA in PBMC obtained from AIH patients (0.131+/-0.046) was lower than that in PBMC of patients with chronic hepatitis C (0.186+/-0.074, p=0.019) and that of healthy subjects (0.188+/-0.060, p=0.013).
The present study of TbetaRII mRNA expression in PBMC from patients with AIH suggested that the decreased expression of TbetaRII might contribute partially to abnormalities in immune regulation observed in patients with AIH, despite concomitant up-regulation of TGF-beta1 production.
背景/目的:为了评估转化生长因子-β1(TGF-β1)的免疫抑制作用与自身免疫性肝炎(AIH)免疫调节异常之间的关联,我们研究了AIH患者外周血单个核细胞(PBMC)中TGF-β1的血清水平和II型TGF-β受体(TβRII)的表达。
本研究纳入了22例AIH患者。使用特异性酶联免疫吸附测定(ELISA)法测定血清总TGF-β1水平。通过针对TβRII的核糖核酸酶(RNase)保护试验半定量测定TβRII mRNA的表达水平。
AIH患者的TGF-β1平均血清水平(230±95 ng/mL)高于健康对照者(137±81 ng/mL,p = 0.012)。AIH患者PBMC中TβRII mRNA的表达水平(0.131±0.046)低于丙型肝炎患者PBMC中的表达水平(0.186±0.074,p = 0.019)以及健康受试者PBMC中的表达水平(0.188±0.060,p = 0.013)。
本研究对AIH患者PBMC中TβRII mRNA表达的研究表明,尽管同时TGF-β1产生上调,但TβRII表达降低可能部分导致了AIH患者观察到的免疫调节异常。