Williams W R, Kagamimori S, Watanabe M, Shinmura T, Hagino N
Clin Exp Immunol. 1983 Sep;53(3):651-8.
Parameters of humoral and cellular immunity were investigated in patients with chronic cadmium (Cd) disease and compared to values in an age matched control group. In the patient group, there was a slight reduction in WBC although T and B lymphocyte ratios were normal. RBC counts were significantly reduced (P less than 0.05). No significant differences in serum immunoglobulin (Ig) concentrations were found. Blood Cd was significantly raised (P less than 0.001) and urine Cd was elevated. In lymphocyte transformation tests, responses to Staphylococcus aureus, PHA and PPD were not impaired and no evidence of Cd hypersensitivity was found. Responses in PHA and ADCC cytotoxicity tests were normal and nitro-blue tetrazolium (NBT) reduction was only slightly decreased in the patient group. beta 2-Microglobulin (beta 2M) was significantly raised in serum (P less than 0.001) and urine (P less than 0.001) of patients. Patient 3 day lymphocyte cultures produced significantly more beta 2M than cultures from the control group (P less than 0.01). beta 2M was increased in lymphocyte cultures, from patient and control groups, containing PHA (P less than 0.01), low Cd concentrations (P less than 0.01) or PPD. The results indicate that chronic Cd disease is not associated with significant alterations in immunological parameters in vitro. The high beta 2M levels associated with this disease may not result entirely from kidney damage but may in part be due to an increase in the release of beta 2M from cells, induced by Cd.
对慢性镉(Cd)病患者的体液免疫和细胞免疫参数进行了研究,并与年龄匹配的对照组的值进行了比较。在患者组中,白细胞略有减少,尽管T和B淋巴细胞比例正常。红细胞计数显著降低(P<0.05)。血清免疫球蛋白(Ig)浓度未发现显著差异。血镉显著升高(P<0.001),尿镉升高。在淋巴细胞转化试验中,对金黄色葡萄球菌、PHA和PPD的反应未受损,未发现镉超敏反应的证据。PHA和ADCC细胞毒性试验的反应正常,患者组硝基蓝四氮唑(NBT)还原仅略有降低。患者血清(P<0.001)和尿液(P<0.001)中的β2-微球蛋白(β2M)显著升高。患者3天淋巴细胞培养物产生的β2M明显多于对照组培养物(P<0.01)。在含有PHA(P<0.01)、低镉浓度(P<0.01)或PPD的患者和对照组淋巴细胞培养物中,β2M增加。结果表明,慢性镉病与体外免疫参数的显著改变无关。与该疾病相关的高β2M水平可能并非完全由肾脏损伤导致,部分可能是由于镉诱导细胞释放β2M增加所致。