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醋酸格拉替雷通过调节适应性免疫细胞来减轻神经病理性痛觉过敏。

Glatiramer acetate attenuates neuropathic allodynia through modulation of adaptive immune cells.

机构信息

Wolfson Centre for Age Related Disease, Kings College London, London, UK.

出版信息

J Neuroimmunol. 2011 May;234(1-2):19-26. doi: 10.1016/j.jneuroim.2011.01.005. Epub 2011 Feb 4.

Abstract

Immune-neuronal interactions contribute to neuropathic pain. Thus, immune-competent cells such as microglia may provide targets for pain relief, as may infiltrating lymphocytes. We evaluated the nature of the lymphocyte response in the spinal cord in association with the maintenance of neuropathic allodynia. We assessed T cell contribution to pain processing by targeting these cells with Glatiramer acetate (GA) which when administered systemically reversed neuropathic allodynia, inhibited microglia response and increased IL-10 and IL-4 expressing T cells in neuropathic dorsal horns. These studies advance understanding of lymphocyte contribution to chronic pain and reveal a new mechanism of T cell intervention.

摘要

免疫-神经元相互作用导致神经病理性疼痛。因此,免疫细胞如小胶质细胞可能成为缓解疼痛的靶点,浸润的淋巴细胞也可能成为靶点。我们评估了与神经病理性痛觉过敏维持相关的脊髓淋巴细胞反应的性质。我们通过用 GA(醋酸格拉替雷)靶向这些细胞来评估 T 细胞对疼痛处理的贡献,GA 全身性给药可逆转神经病理性痛觉过敏,抑制小胶质细胞反应,并增加神经病理性背角中表达 IL-10 和 IL-4 的 T 细胞。这些研究推进了对淋巴细胞对慢性疼痛贡献的理解,并揭示了 T 细胞干预的新机制。

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