Experimental autoimmune encephalomyelitis induction in genetically B cell-deficient mice.
Experimental autoimmune encephalomyelitis induction in genetically B cell-deficient mice.
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DOI：
10.1084/jem.184.6.2271
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发表时间：
1996-12-01
期刊：
影响因子：
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通讯作者：
Janeway CA Jr
中科院分区：
文献类型：
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作者：
Wolf SD;Dittel BN;Hardardottir F;Janeway CA Jr
实验性自身免疫性脑脊髓炎（EAE）是一种由CD 4 T细胞介导的自身免疫性中枢神经系统疾病的动物模型。为了检测B细胞在诱导EAE中的作用，我们使用通过缺失其μ链跨膜区（B10.PLμMT）而使B细胞缺陷的B10.PL（I-Au）小鼠。通过用NH末端髓鞘碱性蛋白致脑炎肽Ac 1 -11免疫B10.PL和B10.PLμMT小鼠，我们观察到在缺乏成熟B细胞的情况下，疾病的发作或严重程度没有差异。然而，与对照组相比，B细胞缺陷小鼠的疾病发作、严重程度、尤其是恢复的变化更大。B10. PL μMT小鼠在缺乏B细胞的情况下很少恢复正常。总而言之，我们的数据表明，B细胞在致脑炎T细胞的激活中不起作用，但可能有助于急性EAE的免疫调节。解释这些影响的机制进行了讨论。
Experimental autoimmune encephalomyelitis (EAE) is an animal model for autoimmune central nervous system disease mediated by CD4 T cells. To examine the role of B cells in the induction of EAE, we used B10.PL (I-Au) mice rendered deficient in B cells by deletion of their μ chain transmembrane region (B10.PLμMT). By immunizing B10.PL and B10.PLμMT mice with the NH-terminal myelin basic protein encephalitogenic peptide Ac1-11, we observed no difference in the onset or severity of disease in the absence of mature B cells. There was, however, a greater variation in disease onset, severity, and especially of recovery in the B cell–deficient mice compared to controls. B10.PLμMT mice rarely returned to normal in the absence of B cells. Taken together, our data suggest that B cells do not play a role in the activation of encephalitogenic T cells, but may contribute to the immune modulation of acute EAE. The mechanisms to explain these effects are discussed.