CXCR3型
神经炎症
四氯化碳
趋化因子
CCR2型
趋化因子受体
小胶质细胞
生物
免疫学
CCL5
免疫系统
细胞生物学
CCL17型
中央控制室4
T细胞
白细胞介素2受体
炎症
作者
Oriane Cédile,Agnieszka Włodarczyk,Trevor Owens
出处
期刊:Apmis
[Wiley]
日期:2017-08-24
卷期号:125 (11): 945-956
被引量:34
摘要
CCL 2 is a chemokine that can be induced during neuroinflammation to recruit immune cells, but its role in the central nervous system ( CNS ) is unclear. Our aim was to better understand its role. We induced CCL 2 in CNS of naive CCL 2‐deficient mice using intrathecally administered replication‐defective adenovirus and examined cell infiltration by flow cytometry. CCL 2 expression induced pronounced and unexpected recruitment of regulatory and IFN γ‐producing T cells to CNS from blood, possibly related to defective egress of monocytes from CCL 2‐deficient bone marrow. Infiltration also occurred in mice lacking CCR 2, a receptor for CCL 2. Expression of another receptor for CCL 2, CCR 4, and CXCR 3, a receptor for CXCL 10, which was also induced, were both increased in CCL 2‐treated CNS . CCR 4 was expressed by neurons and astrocytes as well as CD 4 T cells, and CXCR 3 was expressed by CD 4 and CD 8 T cells. Chemokine‐recruited T cells did not lead to CNS pathology. Our findings show a role for CCL 2 in recruitment of CD 4 T cells to the CNS and show that redundancy among chemokine receptors ensures optimal response.
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