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肺移植排斥反应中的黏附分子(E-选择素和细胞间黏附分子-1)

Adhesion molecules (E-selectin and ICAM-1) in pulmonary allograft rejection.

作者信息

Shreeniwas R, Schulman L L, Narasimhan M, McGregor C C, Marboe C C

机构信息

Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, USA.

出版信息

Chest. 1996 Nov;110(5):1143-9. doi: 10.1378/chest.110.5.1143.

DOI:10.1378/chest.110.5.1143
PMID:8915211
Abstract

Vascular endothelial cells act as antigen-presenting cells in the lung allograft and stimulate alloreactive host lymphocytes. Activated lymphocytes and cytokines can induce expression of leukocyte-endothelial adhesion molecules that facilitate invasion of the allograft by circulating leukocytes. To define the role of endothelial HLA class II antigen and adhesion molecule expression in lung allograft rejection, we prospectively analyzed endothelial expression of HLA class II, E-selectin, and intercellular adhesion molecule-1 (ICAM-1) antigens in 52 transbronchial biopsy specimens from 24 lung allograft recipients as compared to normal control subjects. Thirty-one of 52 specimens showed histologic rejection and 8 of 24 patients developed histologic obliterative bronchiolitis (OB) by the end of the study period. Increased expression of HLA class II antigen was seen in 32 of 52 (62%) lung allograft specimens, but increased expression did not correlate with acute rejection or OB. In contrast, E-selectin expression was seen in 30 of 52 (58%) biopsy specimens and was associated with acute rejection (p < 0.005) and with the development of OB (p < 0.05). Increased expression of ICAM-1 was seen in only 18 of 52 (35%) biopsy specimens and did not correlate with acute rejection or OB. These data suggest that E-selectin expression may be a tissue marker of acute and chronic lung rejection possibly by promoting leukocyte adhesion to the allograft endothelium. The high levels of endothelial HLA class II expression may reflect long-term antigenic stimulation of the allograft even in the absence of rejection.

摘要

血管内皮细胞在肺移植中作为抗原呈递细胞,刺激同种异体反应性宿主淋巴细胞。活化的淋巴细胞和细胞因子可诱导白细胞 - 内皮黏附分子的表达,从而促进循环白细胞对移植肺的侵袭。为了确定内皮细胞 HLA - II 类抗原和黏附分子表达在肺移植排斥反应中的作用,我们前瞻性分析了 24 例肺移植受者的 52 份经支气管活检标本中 HLA - II 类、E - 选择素和细胞间黏附分子 - 1(ICAM - 1)抗原的内皮细胞表达情况,并与正常对照受试者进行比较。在 52 份标本中,有 31 份显示组织学排斥反应,在研究期末,24 例患者中有 8 例发生了组织学闭塞性细支气管炎(OB)。在 52 份肺移植标本中的 32 份(62%)中观察到 HLA - II 类抗原表达增加,但增加的表达与急性排斥反应或 OB 无关。相比之下,在 52 份活检标本中的 30 份(58%)中观察到 E - 选择素表达,且与急性排斥反应(p < 0.005)和 OB 的发生相关(p < 0.05)。在 52 份活检标本中只有 18 份(35%)观察到 ICAM - 1 表达增加,且与急性排斥反应或 OB 无关。这些数据表明,E - 选择素表达可能是急性和慢性肺排斥反应的组织标志物,可能是通过促进白细胞黏附于移植肺内皮。即使在没有排斥反应的情况下,内皮细胞 HLA - II 类高表达可能反映了移植肺的长期抗原刺激。

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Adhesion molecules (E-selectin and ICAM-1) in pulmonary allograft rejection.肺移植排斥反应中的黏附分子(E-选择素和细胞间黏附分子-1)
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