Zhao Shu-Jun, Sun Fu-Jun, Tian En-Jiang, Chen Zu-Pei
Key Lab of Hormone and Development of Ministry of Health, Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, China.
Zhonghua Yu Fang Yi Xue Za Zhi. 2008 Jul;42(7):485-8.
To observe the effects of iodine/selenium on the function of antigen presentation of peritoneal macrophages in rats and explore the immunological mechanisms of iodine/ selenium's role in pathogenesis of autoimmune thyroid diseases (AITD).
Female Lewis rats were randomly divided into four groups including (1) low selenium and normal iodine group (L(sE)N(I)) (2) low selenium and high iodine group (L(Se)H(I)) (3) normal selenium and normal iodine group (N(Se)N(I) ) (4) normal selenium and high iodine group (N(Se)H(I)). All rats were fed by a special diet with lower selenium and iodine in it and drunk ion-free water containing different levels of iodine and selenium for 3 months. Peritoneal macrophages of each group and OVA allergized T cells were prepared and cultured together. Then the function of antigen presentation were estimated by detecting the levels of IL-2 in the culture supernatant. The levels of the expression of co-stimulator CD86 in the spleen of each group were determined by RT-PCR.
The level of IL-2 in the supernatant in N(Se)H(I) (43.22 +/- 3.27) pg/ml was much stronger than N(Se)N(I) [the level of IL-2 was (25.74 +/- 2.45) pg/ml, P < 0.05]. The level of IL-2 in L(Se)N(I) (15.79 +/- 2.13) pg/ml was significantly lower than N(Se)N(I) (P < 0.05). The expression of CD86 mRNA in N(Se)H(I) (CD86/beta-actin: 0.52 +/- 0.10) were higher than N(Se)N(I) (CD86/beta-actin: 0.35 +/- 0.04), P < 0.05.
High iodine could promote the presentation function of macrophages to a higher state than normal. Therefore, high iodine intake might become an importantly inducing factor in thyroid autoimmunity. Low selenium could weaken the ability of recognizing and presenting OVA antigen of peritoneal macrophages which might destroy immunological homeostasis and thus the low selenium intake might also become an inducer of AITD.
观察碘/硒对大鼠腹腔巨噬细胞抗原呈递功能的影响，探讨碘/硒在自身免疫性甲状腺疾病（AITD）发病机制中的免疫作用机制。
将雌性Lewis大鼠随机分为四组：（1）低硒正常碘组（L(sE)N(I)）；（2）低硒高碘组（L(Se)H(I)）；（3）正常硒正常碘组（N(Se)N(I)）；（4）正常硒高碘组（N(Se)H(I)）。所有大鼠均采用含较低硒和碘的特殊饲料喂养，并饮用含不同水平碘和硒的去离子水3个月。制备每组的腹腔巨噬细胞和卵清蛋白（OVA）致敏的T细胞并共同培养。然后通过检测培养上清液中白细胞介素-2（IL-2）的水平来评估抗原呈递功能。采用逆转录-聚合酶链反应（RT-PCR）法检测每组大鼠脾脏中共刺激分子CD86的表达水平。
N(Se)H(I)组培养上清液中IL-2水平为（43.22±3.27）pg/ml，明显高于N(Se)N(I)组[IL-2水平为（25.74±2.45）pg/ml，P<0.05]。L(Se)N(I)组IL-2水平为（15.79±2.13）pg/ml，显著低于N(Se)N(I)组（P<0.05）。N(Se)H(I)组CD86 mRNA表达水平（CD86/β-肌动蛋白：0.52±0.10）高于N(Se)N(I)组（CD86/β-肌动蛋白：0.35±0.04），P<0.05。
高碘可使巨噬细胞的呈递功能提升至高于正常的状态。因此，高碘摄入可能成为甲状腺自身免疫的一个重要诱导因素。低硒可削弱腹腔巨噬细胞识别和呈递OVA抗原的能力，这可能破坏免疫稳态，因此低硒摄入也可能成为AITD的一个诱导因素。
