Department of Biomedical Sciences, College of Osteopathic Medicine, University of New England, 11 Hills Beach Road, Biddeford, ME 04005, USA.
J Neuroimmunol. 2013 Aug 15;261(1-2):37-43. doi: 10.1016/j.jneuroim.2013.04.023. Epub 2013 May 28.
B6 mice infected with LP-BM5 develop severe immunodeficiency (termed murine acquired immunodeficiency syndrome (MAIDS)) and peripheral neuropathy. To determine whether microglial CD40 is involved in LP-BM5-induced peripheral neuropathy, B6-CD40 knockout (KO) mice and B6-CD40 KO mice adoptively transferred either total leukocytes or B cells were examined for behavioral sensitivity, tissue viral loads, cytokine responses, and the development of MAIDS. All three CD40 KO groups developed MAIDS, the severity of which was correlated with peripheral cytokine responses. CD40 KO mice displayed significantly reduced mechanical hypersensitivity post-infection compared to wild-type mice regardless of cell transfer. These findings support microglial CD40 involvement in LP-BM5-induced peripheral neuropathy.
B6 感染 LP-BM5 的小鼠会出现严重的免疫缺陷（称为获得性免疫缺陷综合征（MAIDS））和周围神经病。为了确定小胶质细胞 CD40 是否参与 LP-BM5 诱导的周围神经病，检查了 B6-CD40 敲除（KO）小鼠和 B6-CD40 KO 小鼠过继转移的总白细胞或 B 细胞，以评估行为敏感性、组织病毒载量、细胞因子反应和 MAIDS 的发展。所有三组 CD40 KO 组均发展为 MAIDS，其严重程度与外周细胞因子反应相关。与野生型小鼠相比，无论细胞转移如何，CD40 KO 小鼠在感染后均显示出明显降低的机械性超敏反应。这些发现支持小胶质细胞 CD40 参与 LP-BM5 诱导的周围神经病。
