CCR5 deficiency does not prevent P0 peptide 180-199 immunized mice from experimental autoimmune neuritis
CCR5 deficiency does not prevent P0 peptide 180-199 immunized mice from experimental autoimmune neuritis
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DOI：
10.1016/j.nbd.2004.04.007
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发表时间：
2004-08-01
影响因子：
6.1
通讯作者：
Zhu, J
中科院分区：
文献类型：
--
作者：
Duan, RS;Chen, ZG;Zhu, J
实验性自身免疫性神经炎（Experimental autoimmune neuritis，EAN）是一种周围神经系统炎性自身免疫性脱髓鞘病（inflammatory autoimmune demyelinating disease of peripheral nervous system，PINS），是人类格林-巴利综合征（Guillain-Barre syndrome，GBS）的动物模型。为了探讨CC趋化因子受体5（CCR 5）在EAN炎症过程中的作用，我们用PO蛋白肽180-199在CCR 5缺陷（CCR 5（-/-））小鼠中诱导EAN。我们发现，与CCR 5（-/-）小鼠相比，CCR 5（-/-）小鼠表现出相似的EAN临床病程和严重程度以及EAN马尾（CE）中浸润的巨噬细胞和T细胞特征，并且脾脏单核细胞（MNC）对抗原和有丝分裂原的反应水平相同。（+/+）对照小鼠。然而，在CCR 5（-/-）小鼠中观察到坐骨神经中IP-10和MIP-1 β的产生增加。这些结果表明，CCR 5缺陷不能防止PO肽180-199免疫的小鼠发生EAN。坐骨神经中MIP-1 β和IP-10的增加可能会补偿CCR 5的缺陷，并有助于炎性细胞浸润到PNS。(C)2004爱思唯尔公司All rights reserved.
Experimental autoimmune neuritis (EAN) is an inflammatory autoimmune demyelinating disease of peripheral nervous system (PINS) and represents an animal model of Guillain-Barre syndrome (GBS) in man. The inflammatory cell infiltrating into the PNS is a prerequisite for developing EAN. To explore the role of CC chemokine receptor 5 (CCR5) in the inflammatory process of EAN, we induced EAN in CCR5-deficient (CCR5(-/-)) mice with PO protein peptide 180-199. We found that CCR5(-/-) mice showed a similar EAN clinical course and severity as well as profile of infiltrating macrophages and T cells in cauda equina (CE) of EAN and the same levels of spleen mononuclear cell (MNC) response to antigen and mitogen when compared with CCR5(+/+) control mice. However, increased IP-10 and MIP-1beta production in sciatic nerves were seen in CCR5(-/-) mice. These results suggest that CCR5 deficiency does not prevent PO peptide 180-199-immunized mice from EAN. Increased MIP-1beta and IP-10 in sciatic nerves may compensate the CCR5 deficiency and contribute to inflammatory cells infiltrating to the PNS. (C) 2004 Elsevier Inc. All rights reserved.