Créange A, Barlovatz-Meimon G, Gherardi R K
Groupe d'Etudes et de Recherches sur le Muscle et le Nerf (GERMEN), Faculté de médecine de Créteil, France.
Eur Cytokine Netw. 1997 Jun;8(2):145-51.
Peripheral nerve production of cytokines originates from resident and recruited macrophages, lymphocytes, mastocytes, Schwann cells, and probably neurons. Cytokines are involved in nerve lesions and repair. Tumor necrosis factor-alpha (TNF-alpha) injected into nerve induces Wallerian degeneration, whereas, interleukin-1 (IL-1) production promotes detersion by scavenger macrophages, and synthesis of neurotrophic factors (nerve growth factor-NGF- and leukemia inhibitory factor-LIF). After experimental axotomy, other neurotrophic factors, including IL-6, LIF and transforming growth factor-beta 1 (TGF-beta 1), are overexpressed in nerve and promote axonal growth until axon/Schwann cell contact. Proinflammatory cytokines are instrumental in the course of inflammatory demyelinating neuropathies. They increase vascular permeability and blood nerve barrier breakdown (TNF-alpha, vascular endothelial growth factor/ vascular permeability factor-VEGF/VPF), favor transmigration of leukocytes into nerve, induce activation and proliferation of lymphocytes (IL-1, IL-2) and macrophages (gamma-interferon-IFN-gamma), and have a direct myelinotoxic activity (TNF-alpha and TNF-beta). In addition, downregulation of the immunosuppressive cytokine TGF-beta 1 may favor the nerve inflammatory reactions.
细胞因子在外周神经中的产生源于常驻和募集的巨噬细胞、淋巴细胞、肥大细胞、施万细胞，可能还有神经元。细胞因子参与神经损伤和修复。向神经中注射肿瘤坏死因子-α（TNF-α）可诱导华勒氏变性，而白细胞介素-1（IL-1）的产生通过清道夫巨噬细胞促进清除，并促进神经营养因子（神经生长因子-NGF-和白血病抑制因子-LIF）的合成。实验性轴突切断后，包括IL-6、LIF和转化生长因子-β1（TGF-β1）在内的其他神经营养因子在神经中过度表达，并促进轴突生长直至轴突/施万细胞接触。促炎细胞因子在炎性脱髓鞘性神经病的病程中起作用。它们增加血管通透性和血神经屏障破坏（TNF-α、血管内皮生长因子/血管通透性因子-VEGF/VPF），促进白细胞向神经内迁移，诱导淋巴细胞（IL-1、IL-2）和巨噬细胞（γ-干扰素-IFN-γ）的活化和增殖，并具有直接的髓鞘毒性活性（TNF-α和TNF-β）。此外，免疫抑制细胞因子TGF-β1的下调可能有利于神经炎症反应。
