Voortman Margarete Maria, Greiner Paul, Moser Daniel, Stradner Martin Helmut, Graninger Winfried, Moser Adrian, Haditsch Bernd, Enzinger Christian, Fuchs Siegrid, Fazekas Franz, Fessler Johannes, Khalil Michael
Department of Neurology, Medical University of Graz, Austria.
Division of Rheumatology and Immunology, Medical University of Graz, Austria.
Mult Scler J Exp Transl Clin. 2018 Sep 20;4(3):2055217318800810. doi: 10.1177/2055217318800810. eCollection 2018 Jul-Sep.
The increasing armamentarium of disease-modifying therapies in multiple sclerosis is accompanied by potentially severe adverse effects. The cell-adhesion molecule CD62L, which facilitates leukocyte extravasation, has been proposed as a predictive marker for treatment tolerability. However, pre-analytical procedures might impact test results, thereby limiting its clinical usability. Whether the immediate analysis of CD62L expression of peripheral blood mononuclear cells can aid treatment decision making is yet unclear.
To investigate the effect of various disease-modifying therapies in multiple sclerosis on CD62L expression of CD3CD4 peripheral blood mononuclear cells in freshly collected blood samples.
We collected peripheral blood samples from patients with clinically isolated syndrome and multiple sclerosis (baseline/follow up = 234/ = 98) and healthy controls ( = 51). CD62LCD3CD4 expression was analysed within 1 hour by fluorescence-activated cell sorting.
CD62LCD3CD4 expression was significantly decreased in patients treated with natalizumab ( = 26) and fingolimod ( = 20) and increased with dimethyl-fumarate ( = 15) compared to patients receiving interferon/glatiramer acetate ( = 90/30) or no disease-modifying therapies ( = 53) and controls ( = 51) (<0.001). CD62L expression showed temporal stability during unchanged disease-modifying therapy usage, but increased after natalizumab withdrawal and decreased upon fingolimod introduction.
CD62LCD3CD4 expression is altered in patients treated with different disease-modifying therapies when measured in freshly collected samples. The clinical meaning of CD62L changes under disease-modifying therapies warrants further investigation.
多发性硬化症中疾病修正疗法的不断增加伴随着潜在的严重不良反应。促进白细胞外渗的细胞粘附分子CD62L已被提议作为治疗耐受性的预测标志物。然而，分析前的程序可能会影响检测结果，从而限制其临床可用性。外周血单核细胞CD62L表达的即时分析是否有助于治疗决策尚不清楚。
研究多发性硬化症中各种疾病修正疗法对新鲜采集血样中CD3⁺CD4⁺外周血单核细胞CD62L表达的影响。
我们收集了临床孤立综合征和多发性硬化症患者（基线/随访=234/=98）以及健康对照者（=51）的外周血样本。通过荧光激活细胞分选在1小时内分析CD62L⁺CD3⁺CD4⁺表达。
与接受干扰素/醋酸格拉替雷（=90/30）或未接受疾病修正疗法（=53）的患者以及健康对照者（=51）相比，接受那他珠单抗（=26）和芬戈莫德（=20）治疗的患者中CD62L⁺CD3⁺CD4⁺表达显著降低，而接受富马酸二甲酯（=15）治疗的患者中该表达增加（<0.001）。在疾病修正疗法使用未改变期间，CD62L表达显示出时间稳定性，但在停用那他珠单抗后增加，在引入芬戈莫德后降低。
在新鲜采集的样本中进行检测时，接受不同疾病修正疗法的患者中CD62L⁺CD3⁺CD4⁺表达会发生改变。疾病修正疗法下CD62L变化的临床意义值得进一步研究。
