神经炎症期间靶向CXCL13

Q4 Immunology and Microbiology
A. Huber, D. Irani
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引用次数: 34

摘要

趋化因子C-X-C基序配体13 (CXCL13)在淋巴器官中组成性表达,并控制淋巴细胞和抗原提呈细胞在这些特化结构中的募集和区隔化。然而,最近的数据也发现,在各种情况下,这种分子在中枢神经系统(CNS)炎症过程中也会被诱导。虽然CXCL13在中枢神经系统肿瘤、感染性和自身免疫性疾病发病机制中的作用仍不完全清楚,但一些证据表明,CXCL13可能成为至少其中一些疾病的相关治疗靶点。本文综述了CXCL13如何参与实验动物和人类的特定中枢神经系统疾病的发病机制,特别关注该配体或其受体的阻断是否(以及如果是,如何)可能对宿主有益的问题。目前的阻断策略主要涉及单克隆抗体的使用,但对下游信号通路的更好理解使小分子抑制成为未来的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Targeting CXCL13 During Neuroinflammation.
The chemokine, C-X-C motif ligand 13 (CXCL13), is constitutively expressed in lymphoid organs and controls the recruitment and compartmentalization of lymphocytes and antigen presenting cells within these specialized structures. Recent data, however, also find induction of this molecule during central nervous system (CNS) inflammation under a variety of circumstances. While its role(s) in the pathogenesis of neoplastic, infectious and autoimmune disorders of the CNS remain incompletely understood, several lines of evidence suggest that CXCL13 could become a relevant therapeutic target in at least some of these diseases. This review focuses on how CXCL13 contributes to the pathogenesis of selected CNS disorders involving both experimental animals and humans, paying particular attention to the issue of whether (and if so, how) blockade of this ligand or its receptor might benefit the host. Current blocking strategies largely involve the use of monoclonal antibodies, but an improved understanding of downstream signaling pathways makes small molecule inhibition a future possibility.
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来源期刊
Advances in Neuroimmune Biology
Advances in Neuroimmune Biology Immunology and Microbiology-Immunology
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