Early infiltration of CD8+ macrophages/microglia to lesions of rat traumatic brain injury

Early infiltration of CD8+ macrophages/microglia to lesions of rat traumatic brain injury
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DOI:
10.1016/j.neuroscience.2006.04.027
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发表时间:
2006-01-01
期刊:
影响因子:
3.3
通讯作者:
Schluesener, H. J.
Schluesener, H. J.
中科院分区:
医学3区
文献类型:
--
作者:
Zhang, Z.;Artelt, M.;Schluesener, H. J.

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局部炎症反应在介导创伤性脑损伤的继发性组织损伤中发挥重要作用。有助于受损组织早期浸润的白细胞亚群的特征可能有助于进一步了解病变发展,并有助于确定选择性免疫治疗的细胞靶点。在大鼠脑外伤模型中,损伤后 3 天观察到显着的 CD8(+) 细胞积聚。 CD8(+)细胞严格分布于全坏死区域和全坏死周边。 CD8(+)细胞的形态、积累时间过程和分布与反应性ED1(+)和内皮单核细胞激活性息肉II+小胶质细胞/巨噬细胞相似,但与W3/13(+) T细胞不同。进一步的双标记实验证实 CD8 的主要细胞来源是反应性巨噬细胞/小胶质细胞。这些CD8(+)巨噬细胞/小胶质细胞位于全坏死边界,以及它们内皮单核细胞激活多肽II和P2X(4)受体的共表达都表明它们可能在病变发展中发挥核心作用,因此可能成为免疫治疗、抗炎策略开发的候选者。 (c) 2006 年国际广播组织。由爱思唯尔有限公司出版。保留所有权利。
Local inflammatory responses play an important role in mediating secondary tissue damage in traumatic brain injury. Characterization of leukocytic subpopulations contributing to the early infiltration of the damaged tissue might aid in further understanding of lesion development and contribute to definition of cellular targets for selective immunotherapy. In a rat traumatic brain injury model, significant CD8(+) cell accumulation was observed 3 days post-injury. The CD8(+) cells were strictly distributed to the pannecrotic areas and around the pannecrotic perimeter. The morphology, time course of accumulation and distribution of CD8(+) cells were similar to that of reactive ED1(+) and enclothelial monocyteactivating polypepticle II+ microglia/macrophages, but different from W3/13(+) T cells. Further double-labeling experiments confirmed that the major cellular sources of CD8 were reactive macrophages/microglia. Both the location of these CD8(+) macrophages/microglia to the border of the pannecrosis and their co-expression of endothelial monocyte-activating polypeptide II and P2X(4) receptor suggest they might have a central role in lesion development and might thus be candidates fordevelopment of immunotherapeutic, anti-inflammatory strategies. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.