Ding J-X, Xu L-X, Zhu L, Lv J-C, Zhao M-H, Zhang H, Wang H-Y
Renal Division of Peking University First Hospital, Peking University Institute of Nephrology, Beijing, China.
Scand J Immunol. 2009 Feb;69(2):174-80. doi: 10.1111/j.1365-3083.2008.02204.x.
It is known that aberrant sialylation of IgA1 is involved in the pathogenesis of IgA nephropathy (IgAN). We hypothesize that aberrant sialylation of serum IgA1 may result from changes in the activity of alpha2,6-sialyltransferase (alpha2,6-ST) or expression of its coding gene ST6GALNAC2 in peripheral B lymphocytes. Sixty patients with IgAN and 20 healthy controls were enrolled. Peripheral B lymphocytes were isolated by CD-19-positive magnetic beads. The expression level of ST6GALNAC2 was quantitatively analysed by real-time reverse-transcriptase polymerase chain reaction (PCR). Serum IgA1 and sialylation levels were detected by enzyme-linked immunosorbent assay (ELISA) and specific lectin-binding ELISA. Activity of alpha2,6-ST was measured by specific lectin-binding ELISA. Expression of ST6GALNAC2 in B peripheral lymphocytes was significantly lower in patients with IgAN than that in normal controls (3.7 +/- 2.2 versus 6.3 +/- 2.3, P = 0.016); alpha2,6-ST activity in B lymphocytes was correlated positively with the level of alpha2,6-sialic acid in serum IgA1 in patients (n = 42) and controls (n = 12) (r = 0.37, P = 0.007). However, alpha2,6-ST activity did not differ between patients with IgAN and controls (1.19 +/- 1.43 versus 1.06 +/- 1.17, P > 0.05). These data suggested that reduced sialylation of serum IgA1 may result from decreased expression of ST6GALNAC2. The factors affecting activity of alpha2,6-ST in the sialylation of IgA1 need to be further investigated.
已知IgA1的异常唾液酸化参与了IgA肾病（IgAN）的发病机制。我们推测血清IgA1的异常唾液酸化可能是由于外周B淋巴细胞中α2,6-唾液酸转移酶（α2,6-ST）活性的变化或其编码基因ST6GALNAC2的表达改变所致。招募了60例IgAN患者和20名健康对照者。通过CD-19阳性磁珠分离外周B淋巴细胞。通过实时逆转录聚合酶链反应（PCR）定量分析ST6GALNAC2的表达水平。通过酶联免疫吸附测定（ELISA）和特异性凝集素结合ELISA检测血清IgA1和唾液酸化水平。通过特异性凝集素结合ELISA测量α2,6-ST的活性。IgAN患者外周B淋巴细胞中ST6GALNAC2的表达明显低于正常对照者（3.7±2.2对6.3±2.3，P = 0.016）；患者（n = 42）和对照者（n = 12）中B淋巴细胞中的α2,6-ST活性与血清IgA1中α2,6-唾液酸水平呈正相关（r = 0.37，P = 0.007）。然而，IgAN患者与对照者之间的α2,6-ST活性没有差异（1.19±1.43对1.06±1.17，P> 0.05）。这些数据表明血清IgA1唾液酸化减少可能是由于ST6GALNAC2表达降低所致。影响IgA1唾液酸化中α2,6-ST活性的因素需要进一步研究。
