Gyllemark Paula, Forsberg Pia, Ernerudh Jan, Henningsson Anna J
Department of Infectious Diseases, Region Jönköping County, SE-551 85, Jönköping, Sweden.
Department of Clinical and Experimental Medicine and Department of Infectious Diseases, Linköping University, Linköping, Sweden.
J Neuroinflammation. 2017 Feb 1;14(1):27. doi: 10.1186/s12974-017-0789-6.
B cell immunity, including the chemokine CXCL13, has an established role in Lyme neuroborreliosis, and also, T helper (Th) 17 immunity, including IL-17A, has recently been implicated.
We analysed a set of cytokines and chemokines associated with B cell and Th17 immunity in cerebrospinal fluid and serum from clinically well-characterized patients with definite Lyme neuroborreliosis (group 1, n = 49), defined by both cerebrospinal fluid pleocytosis and Borrelia-specific antibodies in cerebrospinal fluid and from two groups with possible Lyme neuroborreliosis, showing either pleocytosis (group 2, n = 14) or Borrelia-specific antibodies in cerebrospinal fluid (group 3, n = 14). A non-Lyme neuroborreliosis reference group consisted of 88 patients lacking pleocytosis and Borrelia-specific antibodies in serum and cerebrospinal fluid.
Cerebrospinal fluid levels of B cell-associated markers (CXCL13, APRIL and BAFF) were significantly elevated in groups 1, 2 and 3 compared with the reference group, except for BAFF, which was not elevated in group 3. Regarding Th17-associated markers (IL-17A, CXCL1 and CCL20), CCL20 in cerebrospinal fluid was significantly elevated in groups 1, 2 and 3 compared with the reference group, while IL-17A and CXCL1 were elevated in group 1. Patients with time of recovery <3 months had lower cerebrospinal fluid levels of IL-17A, APRIL and BAFF compared to patients with recovery >3 months.
By using a set of markers in addition to CXCL13 and IL-17A, we confirm that B cell- and Th17-associated immune responses are involved in Lyme neuroborreliosis pathogenesis with different patterns in subgroups. Furthermore, IL-17A, APRIL and BAFF may be associated with time to recovery after treatment.
包括趋化因子CXCL13在内的B细胞免疫在莱姆病神经伯氏疏螺旋体病中已明确发挥作用，并且，包括白细胞介素-17A（IL-17A）在内的辅助性T细胞（Th）17免疫最近也被认为与之相关。
我们分析了一组与B细胞和Th17免疫相关的细胞因子和趋化因子，这些样本来自临床特征明确的确诊莱姆病神经伯氏疏螺旋体病患者（第1组，n = 49）的脑脊液和血清，其定义为脑脊液中存在细胞增多症以及脑脊液中有伯氏疏螺旋体特异性抗体；还来自两组可能患有莱姆病神经伯氏疏螺旋体病的患者，分别表现为细胞增多症（第2组，n = 14）或脑脊液中有伯氏疏螺旋体特异性抗体（第3组，n = 14）。一个非莱姆病神经伯氏疏螺旋体病参考组由88名血清和脑脊液中均无细胞增多症及伯氏疏螺旋体特异性抗体的患者组成。
与参考组相比，第1、2和3组脑脊液中B细胞相关标志物（CXCL13、增殖诱导配体（APRIL）和B细胞活化因子（BAFF））水平显著升高，但第3组中的BAFF未升高。关于Th17相关标志物（IL-17A、CXCL1和CC趋化因子配体20（CCL20）），与参考组相比，第1、2和3组脑脊液中的CCL20显著升高，而第1组中的IL-17A和CXCL1升高。恢复时间<3个月的患者脑脊液中IL-17A、APRIL和BAFF水平低于恢复时间>3个月的患者。
通过使用除CXCL13和IL-17A之外的一组标志物，我们证实B细胞和Th17相关免疫反应参与了莱姆病神经伯氏疏螺旋体病的发病机制，且在亚组中有不同模式。此外，IL-17A、APRIL和BAFF可能与治疗后的恢复时间有关。
