Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss
Administration of a monomeric CCL2 variant to EAE mice inhibits inflammatory cell recruitment and protects from demyelination and axonal loss
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DOI：
10.1016/j.jneuroim.2009.01.022
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发表时间：
2009-04-30
影响因子：
3.3
通讯作者：
Martino, G.
中科院分区：
文献类型：
--
作者：
Brini, E.;Ruffini, F.;Martino, G.
基于基因表达数据，我们测试了趋化因子CCL2的P8A-CCL2变体，能够干扰亲本分子的趋化特性，在复发缓解(RR)-EAE SJL中，预防性治疗以剂量依赖的方式显著延迟疾病发作。然而，P8A-CCL2可减少脱髓鞘、轴突损失和中枢神经系统浸润T细胞和巨噬细胞的数量。免疫学分析显示，P8A-CCL2不作用于ag特异性T细胞增殖，也不干扰IFN γ释放效应T细胞的分化。这些结果提示P8A-CCL2的治疗机制可能依赖于对免疫细胞募集的干扰。(C) 2009 Elsevier B.V.版权所有
Based on gene expression data, we tested the P8A-CCL2 variant of the chemokine CCL2, able to interfere with the chemotactic properties of the parental molecule, in relapsing-remitting (RR)-EAE SJL Only preventive treatment significantly delayed disease onset in a dose dependent manner. P8A-CCL2 administration, however, decreased demyelination, axonal loss and number of CNS infiltrating T cells and macrophages. Immunological analysis revealed that P8A-CCL2 does not act on Ag-specific T cell proliferation and does not interfere with the differentiation of IFN gamma-releasing effectors T cells. These results suggest that the therapeutic mechanism of P8A-CCL2 may rely on interference with immune cell recruitment. (C) 2009 Elsevier B.V. All rights reserved.