Features of innate and adaptive immunity in patients with Parkinson's disease

I. Krasakov, N. I. Davydova, Anastasiya A. Kalashnikova, I. Litvinenko, S. Aleksanin, N. Makarova
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Abstract

Introduction. T cells play a significant role in neuroinflammation in Parkinson's disease (PD). Gamma delta T cells are an under-researched 'minor' subpopulation of T cells. An assessment of the immune system in patients with PD, with a focus on Т cells, provides new data on the pathogenesis of neurodegenerative diseases. The aim of the study was to examine the lymphocyte subpopulations, nonclassical Т cells, as well as cytokine production in patients with 3 stage PD complicated by motor fluctuations. Materials and methods. We examined 20 patients with 3 stage PD receiving dopaminergic combination therapy (main group) and 20 age-matched patients with chronic cerebrovascular disease (comparison group). Considering the suspected role of chronic constipation in maintaining dysbiosis and chronic inflammation in patients with PD, the presence of constipation was an inclusion criterion for this study. The subpopulation profile of the peripheral blood lymphocytes was assessed using flow cytofluorometry, as well as cytokine levels using enzyme linked immunosorbent assay. Results. It was found that the number of mature CD3+ T cells with or chains as the T-cell receptors (TCR) in the lymphocyte population was significantly lower in patients with PD median 74% (57.383.5)) than in the comparison group (median 80% (73.086.0); р = 0.014. There was also a statistically significant reduction in the number of CD3+CD56+ natural killer (NK) T cells in the group of patients with PD vs. the comparison group 4.7% (1.37.7) vs. 7.8% (0.824); р = 0.036. At the same time, the number of CD3CD56+ NK cells was significantly higher in the group of patients with PD (16.4% (934)) vs. the comparison group 8.7% (515); р = 0.001. Moreover, the main group had a statistically significantly higher number of activated CD3CD8+ NK cells 7% (4.513.5) vs. the comparison group 3.5% (0.864.9); р 0.001. Out of the total number of Т cells, the TCR CD4+CD8 subpopulation was statistically smaller in the group of patients with PD 13.6% (6.227.0) than in the comparison group 29.8% (4.052.1); р = 0.016. The study of cytokine levels in the group of patients with PD showed a significant increase in the induced production of interleukin-1 (IL-1), as well as a high (aberrant) spontaneous production of IL-10, which was 227.5 pg/ml in patients with PD when the normal range is 023 pg/ml. The correlation analysis showed that the TCR CD4+CD8 subpopulation and cytokines in the group of patients with PD had a statistically significant (p = 0.048) negative correlation with the induced production of IL-10 (r = 0.745) and a significant (p = 0.042) positive correlation with the induced production of the pro-inflammatory cytokine IL-1 (r = 0.648). There was a trend towards increased spontaneous production of IL-10 (r = 0.602; p = 0.0506) as the level of the TCR CD4+CD8 T helper cells decreased. Conclusion. Changes were found in the blood of patients with PD, which indicate a chronic inflammatory process: increased number of CD3CD56+ NK cells, including activated CD3CD8+ cells, and increased production of pro-inflammatory cytokine IL-1 and anti-inflammatory cytokine IL-10. A decrease was found in the level of a minor subpopulation of T cells, TCR CD4+CD8. The correlation found between this subpopulation and the production of pro- and anti-inflammatory cytokines indicates its role in regulation of chronic inflammation in PD.
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帕金森病患者先天免疫和适应性免疫的特点
介绍。T细胞在帕金森病(PD)的神经炎症中起重要作用。γ δ T细胞是一种尚未得到充分研究的T细胞亚群。PD患者免疫系统的评估,以Т细胞为重点,为神经退行性疾病的发病机制提供了新的数据。该研究的目的是检查伴有运动波动的3期PD患者的淋巴细胞亚群、非经典Т细胞以及细胞因子的产生。材料和方法。我们研究了20例接受多巴胺能联合治疗的3期PD患者(主要组)和20例年龄匹配的慢性脑血管疾病患者(对照组)。考虑到慢性便秘在PD患者维持生态失调和慢性炎症中的疑似作用,便秘的存在是本研究的一个纳入标准。使用流式细胞荧光法评估外周血淋巴细胞亚群谱,并使用酶联免疫吸附法评估细胞因子水平。结果。结果发现,PD患者淋巴细胞群中作为T细胞受体(TCR)的成熟CD3+ T细胞数量(中位数74%(57.383.5))显著低于对照组(中位数80% (73.086.0));= 0.014。PD患者组CD3+CD56+自然杀伤(NK) T细胞数量比对照组减少4.7%(1.37.7)比7.8%(0.824),差异有统计学意义;= 0.036。同时,PD患者组CD3CD56+ NK细胞数量(16.4%,934)明显高于对照组(8.7%,515);r = 0.001。主组活化的CD3CD8+ NK细胞数量为7%(4.513.5),高于对照组3.5%(0.864.9),差异有统计学意义;р0.001。在Т细胞总数中,PD患者组的TCR CD4+CD8亚群(13.6%(6.227.0))小于对照组的29.8% (4.052.1);= 0.016。PD患者组细胞因子水平的研究显示,诱导的白细胞介素-1 (IL-1)的产生显著增加,IL-10的自发产生高(异常),PD患者的IL-10的自发产生为227.5 pg/ml,而正常范围为023 pg/ml。相关性分析显示,PD组患者TCR CD4+CD8亚群与细胞因子与诱导IL-10的产生呈显著负相关(p = 0.048),与诱导促炎细胞因子IL-1的产生呈显著正相关(p = 0.042) (r = 0.648)。IL-10的自发生成有增加的趋势(r = 0.602;p = 0.0506), TCR CD4+CD8 T辅助细胞水平降低。结论。PD患者血液中的变化表明了慢性炎症过程:CD3CD56+ NK细胞数量增加,包括活化的CD3CD8+细胞,促炎细胞因子IL-1和抗炎细胞因子IL-10的产生增加。发现T细胞的一个小亚群TCR CD4+CD8水平下降。该亚群与促炎性和抗炎性细胞因子的产生之间的相关性表明其在PD慢性炎症的调节中起作用。
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来源期刊
Annals of Clinical and Experimental Neurology
Annals of Clinical and Experimental Neurology Medicine-Neurology (clinical)
CiteScore
0.80
自引率
0.00%
发文量
32
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