Kao Grace S, Wood Isabelle G, Dorfman David M, Milford Edgar L, Benjamin Richard J
Joint Program in Transfusion Medicine, Harvard Medical School, and the Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Transfusion. 2003 Feb;43(2):185-91. doi: 10.1046/j.1537-2995.2003.00285.x.
TRALI is thought to be triggered by recipient-specific anti-HLA class I or antibodies against neutrophils in donor plasma. Recently, anti-HLA class II have also been implicated. The prevalence of anti-HLA class II was investigated in normal volunteer platelet donors and in two nonfatal TRALI cases utilizing a flow-based assay. Potential target antigens also were investigated.
Commercial flow cytometry-based assays (FlowPRA, One Lambda, Inc.) for anti-HLA class I and II were compared with standard lymphocytotoxicity tests. Subsequently, 151 volunteer platelet donors and two clinical cases of TRALI were screened with FlowPRA. Immunohistochemical studies were performed on lung tissue from a surgical case, an autopsy case, and a fatal TRALI case.
The FlowPRA assays showed moderate concordance for anti-HLA class I (kappa = 0.448) and good concordance for class II antibodies (kappa = 0.801), when compared to standard lymphocytotoxicity assays. Ten and 9 percent of female platelet donors were positive for anti-HLA class I and class II, respectively. Two nonfatal cases of TRALI showed both anti-HLA class I and anti-HLA class II. Immunohistochemical analysis of a TRALI case revealed granulocyte aggregation in alveolar capillaries with activated vascular endothelial cells. HLA class II antigen expression was not present on vascular endothelium or intravascular WBCs; however, strong expression was seen on alveolar macrophages.
FlowPRA assays often detect anti-HLA class I not detected by conventional lymphocytotoxicity assays. These assays reveal anti-HLA class II in normal female donor plasma and in sera implicated in TRALI. Immunohistochemical studies failed to reveal endothelial or intravascular-WBC HLA class II antigen expression in lung tissue derived from TRALI cases or controls, but demonstrated HLA class II expression on pulmonary macrophages.
输血相关急性肺损伤（TRALI）被认为是由受者特异性抗人类白细胞抗原（HLA）I类抗体或供者血浆中的抗中性粒细胞抗体所触发。最近，抗HLA II类抗体也被牵涉其中。利用基于流式细胞术的检测方法，对正常志愿者血小板供者以及两例非致死性TRALI病例中的抗HLA II类抗体患病率进行了调查。同时也对潜在的靶抗原进行了研究。
将基于流式细胞术的商业检测方法（FlowPRA，One Lambda公司）用于检测抗HLA I类和II类抗体，并与标准淋巴细胞毒性试验进行比较。随后，使用FlowPRA对151名志愿者血小板供者和两例TRALI临床病例进行筛查。对一例手术病例、一例尸检病例以及一例致死性TRALI病例的肺组织进行了免疫组织化学研究。
与标准淋巴细胞毒性试验相比，FlowPRA检测方法对抗HLA I类抗体显示出中度一致性（kappa = 0.448），对II类抗体显示出良好一致性（kappa = 0.801）。分别有10%和9%的女性血小板供者抗HLA I类和II类抗体呈阳性。两例非致死性TRALI病例同时显示出抗HLA I类和抗HLA II类抗体。对一例TRALI病例的免疫组织化学分析显示，肺泡毛细血管中有粒细胞聚集，血管内皮细胞被激活。血管内皮或血管内白细胞上未检测到HLA II类抗原表达；然而，在肺泡巨噬细胞上观察到强表达。
FlowPRA检测方法常常能检测到传统淋巴细胞毒性试验未检测出的抗HLA I类抗体。这些检测方法揭示了正常女性供者血浆以及与TRALI相关的血清中的抗HLA II类抗体。免疫组织化学研究未能在TRALI病例或对照的肺组织中揭示内皮或血管内白细胞HLA II类抗原表达，但在肺巨噬细胞上显示出HLA II类表达。
