Leprosy, also known as Hansen’s disease, continues to have a substantial impact on infectious diseases throughout the world. Leprosy is a chronic granulomatous infection caused by Mycobacterium leprae and shows a wide clinical and immunopathological spectrum related to the immune response of the host. This disease affects the skin and other internal organs with a predilection to infect Schwann cells, which play an active role during axonal degeneration, affecting peripheral nerves and promoting neurological damage. This chronic inflammation influences immune function, leading to neuroimmune disorders. Leprosy is also associated with neuroimmune reactions, including type 1 (reverse) and type 2 (erythema nodosum leprosum) reactions, which are immune-mediated inflammatory complications that can occur during the disease and appear to worsen dramatically; these complications are the main concerns of patients. The reactions may induce neuritis and neuropathic pain that progressively worsen with irreversible deformity and disabilities responsible for the immunopathological damage and glial/neuronal death. However, the neuronal damage is not always associated with the reactional episode. Also, the efficacy in the treatment of reactions remains low because of the nonexistence of a specific treatment and missing informations about the immunopathogenesis of the reactional episode. There is increasing evidence that peripheral neuron dysfunction strongly depends on the activity of neurotrophins. The most important neurotrophin in leprosy is nerve growth factor (NGF), which is decreased in the course of leprosy, as well as the presence of autoantibodies against NGF in all clinical forms of leprosy and neuroimmune reactions. The levels of autoantibodies against NGF are decreased by the immunomodulatory activity of cyclosporin A, which mainly controls pain and improves motor function and sensitivity. Therefore, the suppression of anti-NGF and the regulation of NGF levels can be attractive targets for immunomodulatory treatment and for controlling the neuroimmune reactions of leprosy, although further studies are needed to clarify this point.
Neuroimmunomodulation

中文翻译：

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环孢素 A 作为控制神经突和恢复麻风病神经元组织的替代神经免疫策略

麻风病，也称为汉森病，继续对全世界的传染病产生重大影响。麻风病是由麻风分枝杆菌引起的慢性肉芽肿感染并显示出与宿主免疫反应相关的广泛的临床和免疫病理学谱。这种疾病影响皮肤和其他内脏器官，易感染雪旺细胞，雪旺细胞在轴突变性过程中发挥积极作用，影响周围神经并促进神经损伤。这种慢性炎症会影响免疫功能，导致神经免疫疾病。麻风病还与神经免疫反应有关，包括 1 型（反向）和 2 型（麻风结节性红斑）反应，这些反应是免疫介导的炎症并发症，可能在疾病期间发生并且似乎会急剧恶化；这些并发症是患者最关心的问题。这些反应可能会诱发神经炎和神经性疼痛，这些疼痛会随着不可逆的畸形和残疾而逐渐恶化，从而导致免疫病理性损伤和神经胶质/神经元死亡。然而，神经元损伤并不总是与反应发作有关。此外，由于不存在特定的治疗方法以及缺少有关反应事件的免疫发病机制的信息，治疗反应的疗效仍然很低。越来越多的证据表明，周围神经元功能障碍强烈依赖于神经营养因子的活性。麻风病中最重要的神经营养因子是神经生长因子（NGF），它在麻风病过程中减少，并且在所有临床形式的麻风病和神经免疫反应中都存在针对 NGF 的自身抗体。环孢菌素 A 的免疫调节活性降低了针对 NGF 的自身抗体水平，环孢菌素 A 主要控制疼痛并改善运动功能和敏感性。因此，抑制抗 NGF 和调节 NGF 水平可能是免疫调节治疗和控制麻风病神经免疫反应的有吸引力的目标，尽管需要进一步的研究来阐明这一点。
神经免疫调节