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2. Brain Ischemia Induces Diversified Neuroantigen-Specific T-Cell Responses That Exacerbate Brain Injury

Author

Jin, Wei-Na, Gonzales, Rayna, Feng, Yan, Wood, Kristofer, Chai, Zhi, Dong, Jing-Fei, La Cava, Antonio, Shi, Fu-Dong, and Liu, Qiang

Subjects
Brain Disorders, Neurosciences, Autoimmune Disease, Stroke, 1.1 Normal biological development and functioning, Aetiology, Underpinning research, 2.1 Biological and endogenous factors, Neurological, Adoptive Transfer, Animals, Brain, Brain Injuries, Brain Ischemia, Central Nervous System, Humans, Infarction, Middle Cerebral Artery, Mice, Inbred C57BL, Myelin-Oligodendrocyte Glycoprotein, T-Lymphocytes, adaptive immunity, antigen presentation, brain injury, brain ischemia, T-cells, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Neurology & Neurosurgery
Abstract

Background and purposeAutoimmune responses can occur when antigens from the central nervous system are presented to lymphocytes in the periphery or central nervous system in several neurological diseases. However, whether autoimmune responses emerge after brain ischemia and their impact on clinical outcomes remains controversial. We hypothesized that brain ischemia facilitates the genesis of autoimmunity and aggravates ischemic brain injury.MethodsUsing a mouse strain that harbors a transgenic T-cell receptor to a central nervous system antigen, MOG35-55 (myelin oligodendrocyte glycoprotein) epitope (2D2), we determined the anatomic location and involvement of antigen-presenting cells in the development of T-cell reactivity after brain ischemia and how T-cell reactivity impacts stroke outcome. Transient middle cerebral artery occlusion and photothrombotic stroke models were used in this study. We also quantified the presence and status of T cells from brain slices of ischemic patients.ResultsBy coupling transfer of labeled MOG35-55-specific (2D2) T cells with tetramer tracking, we show an expansion in reactivity of 2D2 T cells to MOG91-108 and MOG103-125 in transient middle cerebral artery occlusion and photothrombotic stroke models. This reactivity and T-cell activation first occur locally in the brain after ischemia. Also, microglia act as antigen-presenting cells that effectively present MOG antigens, and depletion of microglia ablates expansion of 2D2 reactive T cells. Notably, the adoptive transfer of neuroantigen-experienced 2D2 T cells exacerbates Th1/Th17 responses and brain injury. Finally, T-cell activation and MOG-specific T cells are present in the brain of patients with ischemic stroke.ConclusionsOur findings suggest that brain ischemia activates and diversifies T-cell responses locally, which exacerbates ischemic brain injury.

Published
2018

3. Potential Protein Signatures for Recurrence Prediction of Ischemic Stroke

Author

Zhang, Chengyi, primary, Liu, Yang, additional, Zhu, Huimin, additional, Huang, Xinying, additional, Guo, Cang, additional, Cheng, Si, additional, Yuan, Meng, additional, Jiang, Yong, additional, Meng, Xia, additional, Johnston, S. Claiborne, additional, Wang, Yongjun, additional, Jin, Wei‐Na, additional, and Shi, Fu‐Dong, additional

Published
2024
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5. APOE from patient-derived astrocytic extracellular vesicles alleviates neuromyelitis optica spectrum disorder in a mouse model

Author

Jiang, Shihe, primary, Li, Xindi, additional, Li, Yan, additional, Chang, Zhilin, additional, Yuan, Meng, additional, Zhang, Ying, additional, Zhu, Huimin, additional, Xiu, Yuwen, additional, Cong, Hengri, additional, Yin, Linlin, additional, Yu, Zhen-Wei, additional, Fan, Junwan, additional, He, Wenyan, additional, Shi, Kaibin, additional, Tian, De-Cai, additional, Zhang, Jing, additional, Verkhratsky, Alexei, additional, Jin, Wei-Na, additional, and Shi, Fu-Dong, additional

Published
2024
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7. Neural stem cells sustain natural killer cells that dictate recovery from brain inflammation

Author

Liu, Qiang, Sanai, Nader, Jin, Wei-Na, La Cava, Antonio, Van Kaer, Luc, and Shi, Fu-Dong

Subjects
Biomedical and Clinical Sciences, Immunology, Neurosciences, Stem Cell Research - Nonembryonic - Non-Human, Transplantation, Regenerative Medicine, Brain Disorders, Stem Cell Research, Aetiology, 2.1 Biological and endogenous factors, Neurological, Aged, Aged, 80 and over, Animals, Brain, Brain Chemistry, Cell Proliferation, Cerebral Ventricles, Cytokines, Encephalitis, Encephalomyelitis, Autoimmune, Experimental, Female, Humans, Immune Tolerance, Interleukin-15, Killer Cells, Natural, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Multiple Sclerosis, Neural Stem Cells, Recovery of Function, Psychology, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Recovery from organ-specific autoimmune diseases largely relies on the mobilization of endogenous repair mechanisms and local factors that control them. Natural killer (NK) cells are swiftly mobilized to organs targeted by autoimmunity and typically undergo numerical contraction when inflammation wanes. We report the unexpected finding that NK cells are retained in the brain subventricular zone (SVZ) during the chronic phase of multiple sclerosis in humans and its animal model in mice. These NK cells were found preferentially in close proximity to SVZ neural stem cells (NSCs) that produce interleukin-15 and sustain functionally competent NK cells. Moreover, NK cells limited the reparative capacity of NSCs following brain inflammation. These findings reveal that reciprocal interactions between NSCs and NK cells regulate neurorepair.

Published
2016

21. sj-pdf-1-jcb-10.1177_0271678X221116048 - Supplemental material for Brain-derived programmed death-ligand 1 mediates immunosuppression post intracerebral hemorrhage

Author

Cheng, Nuo, Wang, Hong, Zou, Ming, Jin, Wei-Na, Shi, Fu-Dong, and Shi, Kaibin

Subjects
110320 Radiology and Organ Imaging, FOS: Clinical medicine, FOS: Biological sciences, Medicine, Cell Biology, 110305 Emergency Medicine, 110306 Endocrinology, Biochemistry, 69999 Biological Sciences not elsewhere classified, 110904 Neurology and Neuromuscular Diseases, Neuroscience
Abstract

Supplemental material, sj-pdf-1-jcb-10.1177_0271678X221116048 for Brain-derived programmed death-ligand 1 mediates immunosuppression post intracerebral hemorrhage by Nuo Cheng, Hong Wang, Ming Zou, Wei-Na Jin, Fu-Dong Shi and Kaibin Shi in Journal of Cerebral Blood Flow & Metabolism

Published
2022
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24. Targeting CCL5 signaling attenuates neuroinflammation after seizure.

Author

Zhang, Zhuoran, Li, Yan, Jiang, Shihe, Shi, Fu‐Dong, Shi, Kaibin, and Jin, Wei‐Na

Subjects
CHEMOKINE receptors, SEIZURES (Medicine), NEUROINFLAMMATION, NEUROLOGICAL disorders, NEURODEGENERATION
Abstract

Background: Epilepsy is a neurological condition that causes unprovoked, recurrent seizures. Accumulating evidence from clinical and experimental studies indicates that neuroinflammation exacerbates seizure activity. Methods: We investigated the transcriptional changes occurring in specific brain domains of a seizure mouse model, using 10× Genomics spatial transcriptomics. Differential gene expression and pathway analysis were applied to investigate potential signaling targets for seizure, including CCL5/CCR5 pathway. Maraviroc, an FDA‐approved C‐C chemokine receptor 5 (CCR5) antagonist, was used to verify the impact of CCL5/CCR5 signaling in seizure mice. Results: We found distinguished regional transcriptome features in the hippocampus of seizure mice. The hippocampus exhibited unique inflammatory gene signatures, including glia activation, apoptosis, and immune response in seizure mice. Especially, we observed notable expression of C‐C chemokine ligand 5 (CCL5) throughout the entire seizure hippocampus. Blockade of CCL5/CCR5 signaling via maraviroc prevented microglia activation and neuron degeneration in seizure mice. Conclusions: This study supports the potential of CCL5/CCR5 signaling for targeting neuroinflammation after seizure. [ABSTRACT FROM AUTHOR]

Published
2023
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26. Additional file 2 of miR-1224 contributes to ischemic stroke-mediated natural killer cell dysfunction by targeting Sp1 signaling

Author

Feng, Yan, Li, Yan, Zhang, Ying, Zhang, Bo-Hao, Zhao, Hui, Zhao, Xin, Shi, Fu-Dong, Jin, Wei-Na, and Zhang, Xiao-An

Abstract

Additional file 2: Supplementary Table 1. miR-1224 inhibits the activation and cytotoxicity of splenic NK cells after ischemic stroke. Flow cytometry was used to analyze the number of functional markers in NK cells. Data are presented as the mean ± SEM. *p < 0.05, **p < 0.01 in mimics versus control; #p < 0.05, ##p < 0.01 in inhibitor versus control; &p < 0.05, &&p < 0.01 in inhibitor versus mimics. Supplementary Table 2. miR-1224 is involved in the alteration of brain-infiltrating NK cells after MCAO. Splenic NK cells isolated from wild-type mice were treated with an miR-1224 control, mimic or inhibitor plasmid. After transfection, NK cells were transferred intravenously into NPG mice before MCAO. The table shows the NK cell counts and the expression of functional markers of NK cells in the ischemic brain. Data are expressed as the mean ± SEM. *p < 0.05, **p < 0.01 in mimics versus control. Supplementary Table 3. miR-1224 negatively regulates NK cell function by modulating Sp1. Flow cytometry shows splenic NK cell counts and functional markers (CD69 and IFN-γ) of wild-type and Sp1-/- mice subjected to MCAO. Data were presented as the mean ± SEM. *p < 0.05 in WT/inhibitor versus WT/vehicle; #p < 0.05 in WT/inhibitor versus Sp1-/-/inhibitor. Supplementary Table 4. miR-1224 negatively regulates NK cell function by modulating Sp1. Flow cytometry shows brain-infiltrating NK cell counts and functional markers (CD69 and IFN-γ) in wild-type and Sp1-/- mice subjected to MCAO. Data and presented as the mean ± SEM.

Published
2021
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37. Reference values for plasma neurofilament light chain (NfL) in healthy Chinese.

Author

Chen, Jingshan, Yang, Xiaoxia, Zhang, Ying, Zheng, Pei, Wei, Changjuan, Mao, Zhifeng, He, Wenyan, and Jin, Wei-Na

Subjects
REFERENCE values, CYTOPLASMIC filaments
Abstract

Plasma concentration of the neurofilament light protein (NFL) is a biomarker of CNS injury in HIV infection: a cross-sectional study. Keywords: biomarker; healthy people; neurofilament light chain; reference values; single-molecular array EN biomarker healthy people neurofilament light chain reference values single-molecular array e153 e156 4 03/13/21 20210401 NES 210401 To the Editor, Identification and quantification of axonal damage contribute to the accurate diagnosis and prognosis assessment for neurological diseases. [Extracted from the article]

Published
2021
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38. Additional file 1: of Infiltration and persistence of lymphocytes during late-stage cerebral ischemia in middle cerebral artery occlusion and photothrombotic stroke models

Author

Feng, Yan, Shiwei Liao, Changjuan Wei, Dongmei Jia, Wood, Kristofer, Liu, Qiang, Xiaoying Wang, Shi, Fu-Dong, and Jin, Wei-Na

Subjects
nervous system, cardiovascular diseases
Abstract

Microglial phenotype at day 14 after photothrombosis and MCAO. C57BL/6 (B6) mice were subjected to sham operation, photothrombosis, or 60 mins MCAO for 14 days. At day 14 after surgery, mice were subjected to flow cytometry assessment. (A) Dot plots of flow cytometry assay show the gating strategy for microglia and CD68-expression. (B) Bar graphs summarize the cumulative data for quantifying microglia population and CD68-expression from brains of photothrombosis- or MCAO-operated mice at 14 days after stroke. n = 4 mice per group. *P

Published
2017
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39. Additional file 2: of Infiltration and persistence of lymphocytes during late-stage cerebral ischemia in middle cerebral artery occlusion and photothrombotic stroke models

Author

Feng, Yan, Shiwei Liao, Changjuan Wei, Dongmei Jia, Wood, Kristofer, Liu, Qiang, Xiaoying Wang, Shi, Fu-Dong, and Jin, Wei-Na

Abstract

Lymphocytes infiltration at day 14 after brain ischemia in ET-1 model. (A) ET-1 model induction. ET-1 and L-NAME were dissolved in sterile saline, and were delivered into the cortex by stereotaxic injection (AP +1.0, ML +1.0, DV -1.0, ET-1 at 1 μg and L-NAME at 2.7 μg). The ipsilateral common carotid artery were permanently occluded just prior to the ET-1 injection. (B) Lymphocyte infiltration at late stage of brain ischemia in mice subjected to ET-1 model. Dot plots of flow cytometry assay show CD4+ T, CD8+ T, NK, and B cells in single cell suspension from brains of sham (PBS injection) or ET-1/L-NAME injected mice at 14 days after procedures. (C) Bar graphs summarize the cumulative data for quantifying CD4+ T, CD8+ T, NK, and B cell counts from brains of ET-1 model at 14 days after stroke. n = 8 mice per group. Error bars represent s.e.m.; *P

Published
2017
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40. Additional file 3: of Infiltration and persistence of lymphocytes during late-stage cerebral ischemia in middle cerebral artery occlusion and photothrombotic stroke models

Author

Feng, Yan, Shiwei Liao, Changjuan Wei, Dongmei Jia, Wood, Kristofer, Liu, Qiang, Xiaoying Wang, Shi, Fu-Dong, and Jin, Wei-Na

Abstract

ROS generation and lymphocytes infiltration in photothrombosis model with lymphocytes pre- or post-stroke transfer. Lymphocytes were isolated from spleens of C57BL/6 mice. 2 × 107 isolated cells were then adoptively transferred into Rag2−/−γc−/− mice followed by sham or photothrombosis procedures, or transferred immediately after procedure. (A) Imaging ROS activity in vivo. Bioluminescent images were captured for 1 min using the cooled IVIS imaging system (Xenogen IVIS-200) after luminol i.p. injection, to monitor the ROS generation in Rag2−/−γc−/− photothrombosis brains. (B) Quantification and statistical analysis of the images. As compared to the pre-stroke cell transfer, post-stroke transferred mice exhibit slightly fewer ROS signal but with no significance. n = 3 mice per group. (C) Lymphocytes were isolated from spleens of C57BL/6 (B6) mice and co-cultured with MIRB. 2 × 107 MIRB-labeled cells were then adoptively transferred into Rag2−/−γc−/− mice followed by sham or stroke procedures, or transferred immediately after procedure. MRI was used to track MIRB-labeled lymphocytes in the ischemic brains of Rag2−/−γc−/− mice. Bar graph shows MIRB signal in mice receiving either sham or photothrombosis model. MIRB signals can be observed in the ischemic brain of post-stroke transferred mice, with comparable intensity to the pre-transferred group. Error bars represent s.e.m.; *P

Published
2017
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47. Colchicine in patients with acute ischaemic stroke or transient ischaemic attack (CHANCE-3): multicentre, double blind, randomised, placebo controlled trial

Author

Li, Jiejie, Meng, Xia, Shi, Fu-Dong, Jing, Jing, Gu, Hong-Qiu, Jin, Aoming, Jiang, Yong, Li, Hao, Johnston, S Claiborne, Hankey, Graeme J, Easton, J Donald, Chang, Liguo, Shi, Penglai, Wang, Lihua, Zhuang, Xianbo, Li, Haitao, Zang, Yingzhuo, Zhang, Jianling, Sun, Zengqiang, Liu, Dongqi, Li, Ying, Yang, Hongqin, Zhao, Jinguo, Yu, Weiran, Wang, Anxin, Pan, Yuesong, Lin, Jinxi, Xie, Xuewei, Jin, Wei-Na, Li, Shuya, Niu, Siying, Wang, Yilong, Zhao, Xingquan, Li, Zixiao, Liu, Liping, Zheng, Huaguang, and Wang, Yongjun

Abstract

ObjectivesTo assess the efficacy and safety of colchicine versus placebo on reducing the risk of subsequent stroke after high risk non-cardioembolic ischaemic stroke or transient ischaemic attack within the first three months of symptom onset (CHANCE-3).DesignMulticentre, double blind, randomised, placebo controlled trial.Setting244 hospitals in China between 11 August 2022 and 13 April 2023.Participants8343 patients aged 40 years of age or older with a minor-to-moderate ischaemic stroke or transient ischaemic attack and a high sensitivity C-reactive protein ≥2 mg/L were enrolled.InterventionsPatients were randomly assigned 1:1 within 24 h of symptom onset to receive colchicine (0.5 mg twice daily on days 1-3, followed by 0.5 mg daily thereafter) or placebo for 90 days.Main outcome measuresThe primary efficacy outcome was any new stroke within 90 days after randomisation. The primary safety outcome was any serious adverse event during the treatment period. All efficacy and safety analyses were by intention to treat.Results4176 patients were assigned to the colchicine group and 4167 were assigned to the placebo group. Stroke occurred within 90 days in 264 patients (6.3%) in the colchicine group and 270 patients (6.5%) in the placebo group (hazard ratio 0.98 (95% confidence interval 0.83 to 1.16); P=0.79). Any serious adverse event was observed in 91 (2.2%) patients in the colchicine group and 88 (2.1%) in the placebo group (P=0.83).ConclusionsThe study did not provide evidence that low-dose colchicine could reduce the risk of subsequent stroke within 90 days as compared with placebo among patients with acute non-cardioembolic minor-to-moderate ischaemic stroke or transient ischaemic attack and a high sensitivity C-reactive protein ≥2 mg/L.Trial registrationClinicalTrials.gov, NCT05439356.

Published
2024
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