Grammer Amrie C, Fischer Randy, Lee Olivia, Zhang Xuan, Lipsky Peter E
B Cell Biology Group in the National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA.
Arthritis Res Ther. 2004;6(1):28-38. doi: 10.1186/ar1155. Epub 2004 Feb 5.
Abnormalities in lymphocyte signaling cascades are thought to play an important role in the development of autoimmune disease. However, the large amount of cellular material needed for standard biochemical assessment of signaling status has made it difficult to evaluate putative abnormalities completely using primary lymphocytes. The development of technology to employ intracellular staining and flow cytometry to assess the signaling status of individual cells has now made it possible to delineate the perturbations that are present in lymphocytes from patients with autoimmune disease. As an example, human B cells from the Ramos B cell line and the periphery of systemic lupus erythematosus (SLE) patients or normal nonautoimmune controls were assessed for activation of the NF-kappaB and mitogen activated protein kinase (MAPK) signaling cascades by intracellular multiparameter flow cytometric analysis and biochemical Western blotting. In combination with fluorochrome conjugated antibodies specific for surface proteins that define B cell subsets, antibodies that recognize activated, or phosphorylated inhibitors of kappaB (IkappaB) as well as the extracellular regulated kinase (ERK), jun N-terminal kinase (JNK) or p38 MAPKs were used to stain fixed and permeabilized human B cells and analyze them flow cytometrically. Examination of the known signaling pathways following engagement of CD40 on human B cells confirmed that intracellular flow cytometry and Western blotting equivalently assay CD154-induced phosphorylation and degradation of IkappaB proteins as well as phosphorylation of the MAPKs ERK, JNK and p38. In addition, B cells from the periphery of SLE patients had a more activated status immediately ex vivo as assessed by intracellular flow cytometric analysis of phosphorylated ERK, JNK and p38 when compared with B cells from the periphery of normal, nonautoimmune individuals. Together, these results indicate that multiparameter intracellular flow cytometric analysis of signaling pathways, such as the NF-kappaB and MAPK cascades, can be used routinely to assess the activation status of a small number of cells and thus delineate abnormalities in signaling molecules expressed in primary lymphocytes from patients with autoimmune disease.
淋巴细胞信号级联异常被认为在自身免疫性疾病的发生发展中起重要作用。然而,用于信号状态标准生化评估所需的大量细胞材料使得使用原代淋巴细胞完全评估假定的异常变得困难。采用细胞内染色和流式细胞术评估单个细胞信号状态的技术发展,现在使得描绘自身免疫性疾病患者淋巴细胞中存在的扰动成为可能。例如,通过细胞内多参数流式细胞术分析和生化蛋白质印迹法,评估来自拉莫斯B细胞系以及系统性红斑狼疮(SLE)患者外周血或正常非自身免疫对照的人B细胞中NF-κB和丝裂原活化蛋白激酶(MAPK)信号级联的激活情况。结合针对定义B细胞亚群的表面蛋白的荧光染料偶联抗体,识别活化的或磷酸化的κB抑制因子(IkappaB)以及细胞外调节激酶(ERK)、c-Jun氨基末端激酶(JNK)或p38 MAPK的抗体被用于对固定和通透处理的人B细胞进行染色,并通过流式细胞术进行分析。对人B细胞上CD40参与后已知信号通路的检测证实,细胞内流式细胞术和蛋白质印迹法等效地检测CD154诱导的IkappaB蛋白磷酸化和降解以及MAPK ERK、JNK和p38的磷酸化。此外,与正常非自身免疫个体外周血的B细胞相比,通过对磷酸化ERK、JNK和p38的细胞内流式细胞术分析评估,SLE患者外周血的B细胞在离体时立即具有更活化的状态。总之,这些结果表明,对NF-κB和MAPK级联等信号通路进行多参数细胞内流式细胞术分析可常规用于评估少量细胞的活化状态,从而描绘自身免疫性疾病患者原代淋巴细胞中表达的信号分子异常情况。