Press R, Pashenkov M, Jin J P, Link H
Neuroimmunology Unit, Neurotec Department, Karolinska Institutet and Department of Neurology, Huddinge University Hospital, Stockholm, Sweden.
J Clin Immunol. 2003 Jul;23(4):259-67. doi: 10.1023/a:1024532715775.
Infiltration of spinal nerve roots and peripheral nerves by macrophages and T cells are rather consistent immunopathologic findings in patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Chemokines play a central role in recruitment of leukocytes to inflamed tissue. Chemokines have been implicated in the pathogenesis of the experimental autoimmune neuritis (EAN), which represents an animal model of GBS, but the role of chemokines in GBS and CIDP is not clear. Since chemokines may be released into CSF from inflamed spinal nerve roots, we studied the concentrations of the chemokines MCP-1, MIP-1beta, MIP-3beta, IP-10, SDF-1alpha, RANTES, and SLC in the CSF by sandwich ELISA in patients over the course of GBS and CIDP, before and after immunomodulatory treatment. Controls consisted of patients with noninflammatory neurological disorders. Patients examined in the acute phase of GBS prior to treatment with intravenous high dose immunoglobulins (IvIg) had elevated CSF levels of MCP-1 (a chemoattractant for blood monocytes and dendritic cells) and IP-10 (a chemoattractant for T cells). Patients with CIDP examined prior to immunomodulatory treatment had elevated CSF levels of MIP-3beta (a chemoattractant for mature dendritic cells, naïve and recently activated T cells) and IP-10. Levels of MIP-3beta tended to decreased during follow-up in those CIDP patients responding favorably to immunomodulatory treatment. CSF levels of MCP-1 and IP-10 correlated with the CSF:plasma albumin ratio in both GBS and CIDP patients. In CIDP patients, CSF levels of MIP-3beta also correlated with the CSF:plasma albumin ratio. These data implicate MCP-1 and IP-10 in the pathogenesis of GBS, and IP-10 and MIP-3beta in the pathogenesis of CIDP.
巨噬细胞和T细胞浸润脊髓神经根和周围神经是吉兰-巴雷综合征（GBS）和慢性炎症性脱髓鞘性多发性神经根神经病（CIDP）患者较为一致的免疫病理学表现。趋化因子在白细胞募集到炎症组织中起核心作用。趋化因子与实验性自身免疫性神经炎（EAN，GBS的一种动物模型）的发病机制有关，但趋化因子在GBS和CIDP中的作用尚不清楚。由于趋化因子可能从炎症脊髓神经根释放到脑脊液中，我们通过夹心ELISA法研究了GBS和CIDP患者在免疫调节治疗前后脑脊液中趋化因子MCP-1、MIP-1β、MIP-3β、IP-10、SDF-1α、RANTES和SLC的浓度。对照组为非炎性神经系统疾病患者。在静脉注射大剂量免疫球蛋白（IvIg）治疗前的GBS急性期患者，脑脊液中MCP-1（血液单核细胞和树突状细胞的趋化因子）和IP-10（T细胞的趋化因子）水平升高。在免疫调节治疗前检查的CIDP患者，脑脊液中MIP-3β（成熟树突状细胞、初始和近期活化T细胞的趋化因子）和IP-10水平升高。在对免疫调节治疗反应良好的CIDP患者随访期间，MIP-3β水平趋于下降。GBS和CIDP患者脑脊液中MCP-1和IP-10水平与脑脊液：血浆白蛋白比值相关。在CIDP患者中，脑脊液中MIP-3β水平也与脑脊液：血浆白蛋白比值相关。这些数据表明MCP-1和IP-10与GBS的发病机制有关，而IP-10和MIP-3β与CIDP的发病机制有关。
