CD5⁺ B-1细胞在实验性自身免疫性脑脊髓炎发病机制中的作用。
Role of CD5+ B-1 cells in EAE pathogenesis.
作者信息
Peterson Lisa K, Tsunoda Ikuo, Fujinami Robert S
机构信息
Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132, USA.
出版信息
Autoimmunity. 2008 Aug;41(5):353-62. doi: 10.1080/08916930801890280.
Abstract
Hybridoma cell lines producing natural autoantibodies (NAA), generated from A.SW mice with progressive experimental autoimmune encephalomyelitis (P-EAE), have been shown to cause demyelination and renal pathology when injected into naive mice. To investigate the relative contribution of these antibodies to disease pathogenesis, B-1 cells, the major producers of NAA, were depleted by hypotonic shock. Depletion of B-1 cells during the effector phase of EAE significantly decreased the severity of demyelination and overall pathology in the brain. There was also a decreased incidence of P-EAE and a decrease in clinical score. Depletion during the induction phase of the disease resulted in an increase in the incidence of P-EAE and in the clinical score. Overall, B-1 cells were found to modulate EAE pathogenesis.
摘要
从患有进行性实验性自身免疫性脑脊髓炎（P-EAE）的A.SW小鼠中产生天然自身抗体（NAA）的杂交瘤细胞系，已被证明注入未感染的小鼠后会导致脱髓鞘和肾脏病变。为了研究这些抗体对疾病发病机制的相对贡献，通过低渗休克耗尽了NAA的主要产生者B-1细胞。在EAE效应期耗尽B-1细胞显著降低了脑内脱髓鞘的严重程度和整体病变。P-EAE的发病率也有所降低，临床评分也下降。在疾病诱导期耗尽B-1细胞导致P-EAE发病率和临床评分增加。总体而言，发现B-1细胞可调节EAE发病机制。
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