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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >T- and B-cell-deficient mice with experimental stroke have reduced lesion size and inflammation.
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T- and B-cell-deficient mice with experimental stroke have reduced lesion size and inflammation.

机译：患有实验性中风的T细胞和B细胞缺陷小鼠的病变面积和炎症减少。

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Stroke induction in immunologically competent mice not only produces local ischemia and brain damage, but also induces early inflammatory changes in brain and peripheral immune responses. Although immune elements clearly are activated after brain vascular occlusion, the relative contribution of T and B lymphocytes to the developing lesion has not been quantified. We evaluated effects 22 h after middle cerebral artery occlusion (90 mins) on histologic injury and peripheral immune activation in severe combined immunodeficient (SCID) mice lacking T and B cells. Cortical and total infarct volumes were strikingly reduced in male SCID mice (n=14, 33+/-4% of contralateral cortex, n=10, 52+/-3% of contralateral hemisphere) versus immunologically intact C57BL/6 mice (wild type, n=9, 57+/-5% of contralateral cortex, 57+/-4% of contralateral hemisphere) (P<0.01). Striatal infarction was not altered (77+/-7% of contralateral striatum in SCID, 84+/-7% in wild type), suggesting that the core of the evolving ischemiclesion was not impacted by lack of T and B cells. As expected, inflammatory factors from immune cells in ischemic SCID brains were essentially absent, with the exception of interleukin-1beta increase in both SCID and wild type tissue. Spleen cell numbers were low in SCID mice, but were further reduced 22 h after stroke, with substantial reduction in most inflammatory factors except for increased expression of interferon-gamma and macrophage inflammatory protein (MIP)-2. These data quantify the damaging effect of T and B lymphocytes on early, evolving ischemic brain injury, and further implicate interleukin-1beta in brain and interferon-gamma and MIP-2 in spleen as inflammatory factors produced by cells other than T and B cells.
机译：具有免疫学能力的小鼠的中风诱导不仅产生局部缺血和脑损伤，而且还引起脑和周围免疫反应的早期炎症变化。尽管脑血管闭塞后免疫元件明显被激活，但是T和B淋巴细胞对正在发展的病变的相对贡献尚未量化。我们评估了大脑中动脉闭塞后22小时（90分钟）对严重缺乏T细胞和B细胞的联合免疫缺陷（SCID）小鼠的组织学损伤和外周免疫激活的影响。与免疫原性完整的C57BL / 6小鼠（野生）相比，雄性SCID小鼠（n = 14，对侧皮质的33 +/- 4％，对侧半球的n = 10，52 +/- 3％）的皮质和总梗塞体积显着减少。类型，n = 9，对侧皮质的57 +/- 5％，对侧半球的57 +/- 4％）（P <0.01）。纹状体梗死没有改变（SCID中对侧纹状体为77 +/- 7％，野生型中为84 +/- 7％），这表明不断发展的局部缺血的核心不受T和B细胞缺乏的影响。如预期的那样，除了SCID和野生型组织中白细胞介素1β的增加外，缺血性SCID脑中免疫细胞的炎症因子基本上不存在。在SCID小鼠中，脾细胞数量少，但在中风后22小时进一步减少，除了增加了干扰素-γ和巨噬细胞炎症蛋白（MIP）-2的表达外，大多数炎症因子均大大减少。这些数据量化了T和B淋巴细胞对早期发展的局部缺血性脑损伤的破坏作用，并进一步暗示大脑中的白介素-1β和脾脏中的干扰素-γ和MIP-2是由T和B细胞以外的细胞产生的炎症因子。

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