Targeting CXCL13 During Neuroinflammation.
Targeting CXCL13 During Neuroinflammation.
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DOI：
10.3233/nib-150101
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发表时间：
2015
影响因子：
--
通讯作者：
Irani DN
中科院分区：
文献类型：
--
作者：
Huber AK;Irani DN
趋化因子C-X-C基序配体13（CXCL 13）在淋巴器官中组成性表达，并控制淋巴细胞和抗原呈递细胞在这些特化结构内的募集和区室化。然而，最近的数据也发现在各种情况下在中枢神经系统（CNS）炎症期间诱导该分子。虽然其在CNS的肿瘤性、感染性和自身免疫性病症的发病机制中的作用仍不完全清楚，但几条证据表明，CXCL 13可以成为至少一些这些疾病中的相关治疗靶标。本文综述了CXCL 13如何有助于选定的中枢神经系统疾病的发病机制，涉及实验动物和人类，特别注意的问题是否（如果是这样，如何）封锁这种配体或其受体可能有利于主机。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。
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.