论文部分内容阅读
通过观察狼疮性肾炎（ＬＮ）患者淋巴细胞及粘附分子变化，探讨ＬＮ发病机制。方法采用流式细胞术及免疫荧光双染色法，检测３５例ＬＮ患者淋巴细胞及粘附分子表型（ＣＤ３、ＣＤ４、ＣＤ８、ＣＤ２０、ＣＤ４５ＲＡ、ＣＤ４５ＲＯ、ＣＤ１１ａ、ＣＤ１８、ＣＤ５４）。结果ＬＮ活动期ＣＤ８＋细胞增高；ＣＤ４＋ＣＤ４５ＲＡ＋细胞降低；ＣＤ８＋ＣＤ４５ＲＡ＋及ＣＤ８＋ＣＤ４５ＲＯ＋细胞增高。此外ＣＤ４＋细胞表面ＣＤ１１ａ（ＬＦＡ－１α）和ＣＤ１８（ＬＦＡ－１β）降低；后二者在ＣＤ８＋细胞上增高；作为二者配体的ＣＤ５４（细胞间粘附分子１，ＩＣＡＭ－１）亦在ＣＤ２０＋细胞上增高。ＣＤ８＋细胞上的ＣＤ１８增高与ＣＤ４＋ＣＤ４５ＲＡ＋细胞降低呈负相关（Ｐ＜０．０５）与ＣＤ２０＋细胞上的ＣＤ５４增高呈正相关（Ｐ＜０．０１）。结论Ｔ细胞（ＣＤ８＋）与Ｂ细胞（ＣＤ２０＋）的ＣＤ１１α／ＣＤ１８与ＣＤ５４表达紊乱，提示粘附分子在ＬＮ发病机制中可能具有重要作用
To investigate the pathogenesis of LN by observing the changes of lymphocytes and adhesion molecules in patients with lupus nephritis (LN). Methods Flow cytometry and immunofluorescence double staining were used to detect the lymphocyte and adhesion molecule phenotypes in 35 patients with LN (CD3, CD4, CD8, CD20, CD45RA, CD45RO, CD11a, CD18 and CD54). Results LN active stage CD8 + cells increased; CD4 + CD45RA + cells decreased; CD8 + CD45RA + and CD8 + CD45RO + cells increased. In addition, the expression of CD11a (LFA-1α) and CD18 (LFA-1β) on the surface of CD4 + cells decreased; the latter two increased on CD8 + cells; CD54 (ICAM- Increased cells. The increase of CD18 on CD8 + cells was negatively correlated with the decrease of CD4 + CD45RA + cells (P <0.05) and positively correlated with the increase of CD54 on CD20 + cells (P <0.01). Conclusions The expression of CD11α / CD18 and CD54 in T cells (CD8 +) and B cells (CD20 +) is disturbed, suggesting that adhesion molecules may play an important role in the pathogenesis of LN