Journal of neuroimmunology最新文献

Chronic g-CSF increases the neutrophil-lymphocyte ratio and decreases plasma corticosterone concentrations in Peromyscus maniculatus without impacting compulsive-like stereotypy 慢性 g-CSF 可提高中性粒细胞-淋巴细胞比率，降低啮齿类动物血浆皮质酮浓度，但不会影响强迫性刻板行为

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-11-25 DOI: 10.1016/j.jneuroim.2024.578490

J.P. Strydom, Linda Brand, Francois P. Viljoen, De Wet Wolmarans

Increasing evidence points to brain-immune mechanisms underlying conditions characterized by neurocognitive rigidity. However, causal evidence remains elusive. Thus, the present work first aimed to investigate the naturalistic associations between rigid motor stereotypy and non-specific markers of systemic inflammation, i.e., the neutrophil-lymphocyte ratio (NLR) and plasma corticosterone concentrations in deer mice. We then explored causal immune-brain interactions by bolstering the NLR, using the recombinant human granulocyte colony-stimulating factor (g-CSF), i.e., pegfilgrastim (Peg). One-hundred and twenty (120) 3-week-old deer mice (both sexes) were exposed to nine weekly injections with normal water for injection or Peg (n = 60 per group) and then assessed for stereotypical expression. Stereotypical behaviour, the NLR, and plasma corticosterone were then measured. Our findings show that 1) NLR and plasma corticosterone concentrations do not predict stereotypical expression and 2) chronic Peg exposure significantly increased the NLR and decreased the plasma corticosterone concentration in mice of both sexes, without impacting stereotypical expression. While valuable findings related to the relationship between exogenous NLR manipulation and immune system functioning were highlighted, continued investigation will be necessary to further explore whether spontaneous stereotypy in deer mice may be associated with immune-inflammatory involvement.

越来越多的证据表明，以神经认知僵化为特征的疾病背后存在大脑免疫机制。然而，因果关系的证据仍然难以捉摸。因此，本研究首先旨在调查鹿小鼠僵化运动刻板性与全身炎症的非特异性标志物（即中性粒细胞-淋巴细胞比率（NLR）和血浆皮质酮浓度）之间的自然关联。然后，我们利用重组人粒细胞集落刺激因子（g-CSF），即 pegfilgrastim（Peg），通过增强 NLR 来探索免疫与大脑之间的因果相互作用。对120只3周大的鹿小鼠（雌雄均可）每周注射9次普通注射用水或Peg（每组60只），然后评估其刻板行为表现。然后测量鹿小鼠的刻板行为、NLR 和血浆皮质酮。我们的研究结果表明：1）NLR 和血浆皮质酮浓度不能预测刻板行为的表现；2）长期暴露于 Peg 会显著增加雌雄小鼠的 NLR 和降低血浆皮质酮浓度，但不会影响刻板行为的表现。尽管研究人员强调了外源 NLR 操作与免疫系统功能之间关系的宝贵发现，但仍有必要继续进行研究，以进一步探讨鹿小鼠的自发刻板行为是否可能与免疫炎症参与有关。

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引用次数: 0

The role of the immune system in Parkinson's disease pathogenesis: A focus on Th17 cells - A systematic review and meta-analysis 免疫系统在帕金森病发病机制中的作用：聚焦Th17细胞--系统综述与荟萃分析。

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-11-17 DOI: 10.1016/j.jneuroim.2024.578484

Zihan Jiang , Honghao Huang , Yiqun Chen , Haobo Xie , Yangguang Lu , Yaoyin Ge , Ruotong Yao , Lingsheng Wang , Zihao Wu , Yiran Bu , Guangyong Chen , Dehao Yang

Background

Parkinson's disease (PD) has been linked to T helper 17 (Th17) cells in prior investigations, but the evidence remains inconclusive. To gain a deeper understanding of this potential connection, we conducted a systematic review and meta-analysis.

Methods

A comprehensive search for relevant studies published up to July 8, 2023, was performed across PubMed, EMBASE, and Cochrane Library databases. A random-effect model was employed to synthesize effect sizes and their corresponding 95 % confidence intervals (CIs). Leave-one-out sensitivity analysis and funnel plots with trim-and-fill were utilized to assess the combined results' robustness.

Results

Thirteen studies were ultimately included in the meta-analysis. Pooled effect sizes indicated a significantly higher percentage of Th17 cells in PD patients (Standardized Mean Difference [SMD] = 1.00, 95 % CI 0.30–1.71). Notably, Th17 cell levels were more elevated in Asian PD patients (SMD = 1.33, 95 % CI 0.31–2.35). Additionally, the percentage of Th17 cells positively correlated with Movement Disorder Society Unified Parkinson's Disease Rating Scale-III (UPDRS-III) scores (r = 0.22, 95 % CI 0.01–0.41), indicating a link to motor dysfunction. Conversely, a negative correlation was observed with Cognitive function scale scores (r = − 0.27, 95 % CI -0.47–-0.04), suggesting a potential association with cognitive decline.

Conclusions

This study revealed a positive association between Th17 cells and PD, with PD patients exhibiting elevated Th17 levels. Furthermore, the percentage of Th17 cells correlated with motor and cognitive impairments in PD patients.

背景：先前的研究发现帕金森病（PD）与T辅助细胞17（Th17）有关，但证据仍不确定。为了深入了解这种潜在的联系，我们进行了一项系统回顾和荟萃分析：方法：我们在 PubMed、EMBASE 和 Cochrane Library 数据库中全面检索了截至 2023 年 7 月 8 日发表的相关研究。采用随机效应模型合成效应大小及其相应的 95% 置信区间 (CI)。为了评估综合结果的稳健性，采用了留空敏感性分析和带有修剪填充功能的漏斗图：荟萃分析最终纳入了 13 项研究。汇总效应大小表明，PD 患者的 Th17 细胞比例明显更高（标准化均值差 [SMD] = 1.00，95 % CI 0.30-1.71）。值得注意的是，亚裔帕金森病患者的 Th17 细胞水平更高（SMD = 1.33，95 % CI 0.31-2.35）。此外，Th17细胞的百分比与运动障碍协会统一帕金森病量表-III（UPDRS-III）评分呈正相关（r = 0.22，95 % CI 0.01-0.41），表明与运动功能障碍有关。相反，与认知功能量表评分呈负相关（r = - 0.27，95 % CI -0.47--0.04），表明可能与认知功能下降有关：本研究揭示了Th17细胞与帕金森病之间的正相关，帕金森病患者的Th17细胞水平升高。此外，Th17细胞的百分比与帕金森病患者的运动和认知障碍相关。

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引用次数: 0

Immune cell-enriched single-cell RNA sequencing unveils the interplay between infiltrated CD8+ T resident memory cells and choroid plexus epithelial cells in Alzheimer's disease 免疫细胞富集单细胞 RNA 测序揭示了阿尔茨海默病中浸润的 CD8+ T 常驻记忆细胞与脉络丛上皮细胞之间的相互作用。

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-11-17 DOI: 10.1016/j.jneuroim.2024.578488

Seong-Jun Kang , Yong-Hee Kim , Thuy Nguyen-Phuong , Yijoon Kim , Jin-Mi Oh , Jae-chun Go , DaeSik Kim , Chung-Gyu Park , Hyunsu Lee , Hyun Je Kim

Alzheimer's disease (AD) is a progressive neurological disorder and the leading cause of dementia. Despite significant efforts, treatment strategies targeting amyloid-β have been less successful than anticipated. Recently, the role of neuroinflammation and adaptive immune response in AD pathogenesis has gained attention. Here, we performed immune cell-enriched single-cell RNA sequencing of brain parenchymal cells from 12-month-old 5xFAD, an AD mouse model. We analyzed 11,587 single cells and found distinct differences in T cell and choroid plexus cell populations between 5xFAD mouse and littermate control. Subsequent sub-clustering of T cells in the 5xFAD mouse revealed distinct subtypes, with CD8⁺ resident memory T cells (T_RM) being the most prevalent T cell type. In addition, we observed an increase in T cell exhaustion markers, including Pdcd1, Ctla4, and Havcr2, with a particularly significant elevation of PD-1 and TIM-3 in CD8⁺ T_RM in 5xFAD mouse. Furthermore, choroid plexus (ChP) epithelial cells showed altered gene expression patterns, with higher expression of MHC class I and Type I IFN-stimulated genes in 5xFAD mouse compared to the control mouse, suggesting an association with clonal expansion of AD-specific T cells in the brain. Through single-cell RNA sequencing (scRNA-seq) analysis, our study highlights the potential role of resident memory CD8⁺ T cell and their possible interactions with ChP epithelial cells. This study provides an exploration of the brain microenvironment landscape in AD, revealing critical insights into its underlying mechanisms.

阿尔茨海默病（AD）是一种进行性神经系统疾病，也是导致痴呆症的主要原因。尽管做出了巨大的努力，但针对淀粉样蛋白-β的治疗策略并没有预期的那么成功。最近，神经炎症和适应性免疫反应在AD发病机制中的作用受到了关注。在这里，我们对12个月大的5xFAD（一种AD小鼠模型）脑实质细胞进行了免疫细胞富集单细胞RNA测序。我们分析了 11,587 个单细胞，发现 5xFAD 小鼠与同窝对照小鼠的 T 细胞和脉络丛细胞群存在明显差异。我们随后对 5xFAD 小鼠的 T 细胞进行了分组，发现了不同的亚型，其中 CD8+ 常驻记忆 T 细胞（TRM）是最普遍的 T 细胞类型。此外，我们还观察到 T 细胞衰竭标记物的增加，包括 Pdcd1、Ctla4 和 Havcr2，尤其是 5xFAD 小鼠 CD8+ TRM 中 PD-1 和 TIM-3 的显著升高。此外，脉络丛（ChP）上皮细胞的基因表达模式也发生了改变，与对照组小鼠相比，5xFAD小鼠的MHC I类基因和I型IFN刺激基因的表达量更高，这表明与AD特异性T细胞在大脑中的克隆扩增有关。通过单细胞 RNA 测序（scRNA-seq）分析，我们的研究强调了常驻记忆 CD8+ T 细胞的潜在作用及其与 ChP 上皮细胞的可能相互作用。这项研究探索了AD的大脑微环境状况，揭示了其潜在机制的重要见解。

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引用次数: 0

Retinoic acid modulates peripheral blood helper innate lymphoid cell composition in vitro in patients with multiple sclerosis 维甲酸可调节多发性硬化症患者体外外周血辅助性先天性淋巴细胞的组成。

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-11-17 DOI: 10.1016/j.jneuroim.2024.578489

Altuğ Özkoşar , Fatma Betül Öktelik , Metin Yusuf Gelmez , Sevda Öztürk Erden , Tuncay Gündüz , Murat Kürtüncü , Günnur Deniz , Suzan Çınar

This study investigates the frequency and numbers of circulating helper innate lymphoid cells (ILCs) in untreated relapsing-remitting multiple sclerosis (RRMS) patients, focusing on intracellular IL-10 and CCR6 expressions under IL-2, IL-33, and retinoic acid (RA) stimulation in vitro and their associations with clinical features in RRMS. In RRMS patients, ILC1 levels were notably higher upon IL-2 + IL-33 + RA stimulation, while ILC2 levels, particularly the c-Kit⁺ ILC2 and CCR6⁺ ILC2 subsets, were significantly lower compared to unstimulated conditions. Additionally, IL-10⁺ ILC1 levels were elevated. The ratios of IL-10⁺ ILC1/ILC1, c-Kit⁺ ILC2/c-Kit⁻ ILC2, and CCR6⁺ ILC2/ILC2 were associated with the progression index (PI) in RRMS patients.

本研究调查了未经治疗的复发缓解型多发性硬化症（RRMS）患者体内循环辅助性先天性淋巴细胞（ILC）的频率和数量，重点研究了体外IL-2、IL-33和维甲酸（RA）刺激下细胞内IL-10和CCR6的表达及其与RRMS临床特征的关系。在RRMS患者中，IL-2+IL-33+RA刺激下ILC1水平明显升高，而ILC2水平，尤其是c-Kit+ ILC2和CCR6+ ILC2亚群，与非刺激条件下相比明显降低。此外，IL-10+ ILC1 水平升高。IL-10+ ILC1/ILC1、c-Kit+ ILC2/c-Kit- ILC2和CCR6+ ILC2/ILC2的比率与RRMS患者的病情进展指数（PI）相关。

引用次数: 0

Silencing of circular RNA PTP4A2 ameliorates depressive-like behaviors by inhibiting microglia activation in mice 通过抑制小鼠小胶质细胞的激活，沉默环状 RNA PTP4A2 可改善抑郁样行为。

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-11-13 DOI: 10.1016/j.jneuroim.2024.578486

Han Zhang, Xiang Chen, Jialu Qian

Major depressive disorder (MDD) is a prevalent mental illness and showed a strong link with inflammation. Microglia, as the main resident immune cells, play an important role in the occurrence and development of depression. Circular RNA PTP4A2 (circPTP4A2) was highly expressed in microglia inflammation induced by oxygen glucose deprivation/reperfusion. However, whether circPTP4A2 involves in microglia inflammation in MDD is not clear. Here, chronic unpredictable stress (CUS) induced depressive behaviors and microglia activation in mouse hippocampus, accompanied by the elevated expression of circPTP4A2. Knockdown circPTP4A2 in mouse hippocampus ameliorated depressive-like behaviors and microglia activation. Moreover, CUS promoted phosphorylation of ERK, JNK and P38 in mouse hippocampus as same as LPS-exposed BV2 microglia. Only P38 phosphorylation was inhibited by circPTP4A2 knockdown in the hippocampus. P38 inhibitor, sb203580, repressed circPTP4A2 overexpression-induced inflammatory reaction in BV2 cells. These findings suggest that circPTP4A2 promotes depressive-like behaviors and microglia activation via P38 phosphorylation.

重度抑郁症（MDD）是一种常见的精神疾病，与炎症有着密切的联系。小胶质细胞作为主要的常驻免疫细胞，在抑郁症的发生和发展中扮演着重要角色。环状 RNA PTP4A2（circPTP4A2）在氧葡萄糖剥夺/再灌注诱导的小胶质细胞炎症中高表达。然而，circPTP4A2是否参与了MDD中的小胶质细胞炎症尚不清楚。在这里，慢性不可预知应激（CUS）诱导了小鼠海马的抑郁行为和小胶质细胞活化，并伴随着circPTP4A2的表达升高。在小鼠海马中敲除circPTP4A2可改善抑郁样行为和小胶质细胞活化。此外，CUS 与 LPS 暴露的 BV2 小胶质细胞一样，促进了小鼠海马中 ERK、JNK 和 P38 的磷酸化。在海马中，只有 P38 磷酸化被 circPTP4A2 敲除抑制。P38 抑制剂 sb203580 可抑制 circPTP4A2 过表达诱导的 BV2 细胞炎症反应。这些发现表明，circPTP4A2通过P38磷酸化促进抑郁样行为和小胶质细胞活化。

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引用次数: 0

Pre-existing Lambert-Eaton Myasthenic Syndrome and Scleroderma in a Patient with Neuroendocrine Carcinoma Undergoing Immune Checkpoint Inhibitor Cancer Immunotherapy 接受免疫检查点抑制剂癌症免疫疗法的神经内分泌癌患者原有的兰伯特-伊顿氏肌萎缩综合征和硬皮病

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-11-12 DOI: 10.1016/j.jneuroim.2024.578485

Nisa Vorasoot , Thorvardur R. Halfdanarson , Nicolas N. Madigan , Divyanshu Dubey , Uma Thanarajasingam , Anastasia Zekeridou

Introduction

Paraneoplastic neurological syndromes (PNS) can worsen with immune checkpoint inhibitor (ICI) cancer immunotherapy.

Case report

A 66-year-old female with paraneoplastic Lambert-Eaton Myasthenic Syndrome (LEMS), which led to the diagnosis of metastatic neuroendocrine carcinoma, was treated with intravenous immune globulin (IVIg) (with minimal response), chemotherapy, and radiation, resulting in neurological improvement. However, sclerodermatous changes developed after a year. Due to cancer progression, dual ICI therapy was initiated, and the patient remained stable for eight months until the progression of both LEMS and cancer, ultimately leading to death.

Discussion

This case highlights the challenges of managing pre-existing PNS during ICI therapy, emphasizing the need for a multidisciplinary approach and the consideration of unusual clinical presentations in therapeutic decision-making.

导言：副肿瘤性神经综合征（PNS）会随着免疫检查点抑制剂（ICI）癌症免疫疗法而恶化：一名66岁的女性患者患有副肿瘤性兰伯特-伊顿肌萎缩综合征（LEMS），诊断为转移性神经内分泌癌，患者接受了静脉注射免疫球蛋白（IVIg）（反应微弱）、化疗和放疗，神经系统症状有所改善。然而，一年后出现了硬皮病变。由于癌症进展，患者开始接受双 ICI 治疗，病情稳定了八个月，直到 LEMS 和癌症同时进展，最终导致死亡：本病例凸显了在 ICI 治疗期间管理原有 PNS 所面临的挑战，强调了多学科方法的必要性，以及在治疗决策中考虑异常临床表现的必要性。

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引用次数: 0

MOGAD presenting as fulminant intracranial hypertension 表现为暴发性颅内高压的 MOGAD。

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-11-10 DOI: 10.1016/j.jneuroim.2024.578487

Sai Nagaratnam , Amardeep Gill , Niroshan Jeyakumar , Shuo Xi , Ming-Wei Lin , Andrew Martin , Winny Varikatt , Michael W.K. Fong , Hugo Morales-Briceno

Objectives

Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) has an expanding phenotype. We describe two cases of MOGAD with associated severe intracranial hypertension.

Case 1: A 21-year-old male presented with diffuse cortical encephalitis and intracranial hypertension with both serum and CSF MOG antibody positivity. Initial brain CT scan was normal but subsequent demyelination was evident on MRI. Case 2: A 44-year-old female presented with a progressive brainstem encephalitis and intracranial hypertension and normal MRI, with later development of subcortical demyelination which was confirmed on brain biopsy. CSF-restricted MOG antibody was detected following the biopsy results.

Results

Both patients presented with clinical features of severe intracranial hypertension requiring surgical management followed by immunosuppressive therapy (methylprednisone and plasma exchange; and intravenous immunoglobulin and plasma exchange) leading to clinical improvement.

Discussion

MOGAD should be in the differential diagnosis of acute severe intracranial hypertension even in the absence of demyelination on initial neuroimaging. Clinicians should be alert of this syndrome that requires combined management of intracranial pressure in addition to early and intensive immunotherapy.

目的：髓鞘少突胶质细胞糖蛋白抗体病（MOGAD）的表型不断扩大。我们描述了两例伴有严重颅内高压的 MOGAD 病例。病例 1：21 岁男性，弥漫性皮质脑炎和颅内高压，血清和脑脊液 MOG 抗体均阳性。最初的脑 CT 扫描结果正常，但随后的核磁共振检查发现脱髓鞘现象明显。病例 2：一名 44 岁女性患者出现进行性脑干脑炎和颅内高压，核磁共振成像正常，后来出现皮层下脱髓鞘，脑活检证实了这一点。活检结果出来后，检测到了脑脊液限制性 MOG 抗体：结果：两名患者均表现为严重颅内高压的临床特征，需要手术治疗，随后接受免疫抑制治疗（甲基强的松和血浆置换；静脉注射免疫球蛋白和血浆置换），临床症状有所改善：讨论：即使最初的神经影像学检查没有发现脱髓鞘，MOGAD 也应作为急性重度颅内高压的鉴别诊断之一。临床医生应警惕这种综合征，除了早期强化免疫治疗外，还需要对颅内压进行综合管理。

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引用次数: 0

Minocycline inhibits microglial activation in the CA1 hippocampal region and prevents long-term cognitive sequel after experimental cerebral malaria 米诺环素可抑制 CA1 海马区的小胶质细胞活化并预防实验性脑疟疾后的长期认知后遗症

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-10-29 DOI: 10.1016/j.jneuroim.2024.578480

E.T. Moreira , M.P. Lourenço , T. Cunha-Fernandes , T.I. Silva , L.D. Siqueira , H.C. Castro-Faria-Neto , P.A. Reis

Cerebral malaria is the worst complication of malaria infection, has a high mortality rate, and may cause different neurodysfunctions, including cognitive decline. Neuroinflammation is an important cause of cognitive damage in neurodegenerative diseases, and microglial cells can be activated in a disease-associated profile leading to tissue damage and neuronal death. Here, we demonstrated that treatment with minocycline reduced blood-brain barrier breakdown and modulated ICAM1 mRNA expression; reduced proinflammatory cytokines, such as TNF-α, IL-1β, IFN-γ, and IL-6; and prevented long-term cognitive decline in contextual and aversive memory tasks. Taken together, our data suggest that microglial cells are activated during experimental cerebral malaria, leading to neuroinflammatory events that end up in cognitive damage. In addition, pharmacological modulation of microglial activation, by drugs such as minocycline may be an important therapeutic strategy in the prevention of long-term memory impairment.

脑疟疾是疟疾感染最严重的并发症，死亡率很高，并可能导致不同的神经功能障碍，包括认知能力下降。神经炎症是神经退行性疾病中认知损伤的重要原因，小胶质细胞可在疾病相关的情况下被激活，导致组织损伤和神经元死亡。在这里，我们证明了米诺环素治疗可减少血脑屏障的破坏并调节ICAM1 mRNA的表达；减少促炎细胞因子，如TNF-α、IL-1β、IFN-γ和IL-6；以及防止情境记忆和厌恶记忆任务中的长期认知能力下降。总之，我们的数据表明，小胶质细胞在实验性脑疟疾期间被激活，导致神经炎症事件，最终造成认知损伤。此外，米诺环素等药物对小胶质细胞活化的药理调节可能是预防长期记忆损伤的重要治疗策略。

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引用次数: 0

Influence of cocaine use reduction on markers of immune function 减少使用可卡因对免疫功能指标的影响

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-10-28 DOI: 10.1016/j.jneuroim.2024.578470

William W. Stoops , Thomas P. Shellenberg , Sean D. Regnier , David H. Cox , Reuben Adatorwovor , Lon R. Hays , Danielle M. Anderson , Joshua A. Lile , Joy M. Schmitz , Jennifer R. Havens , Suzanne C. Segerstrom

This study determined the effects of reduced cocaine use on immune function. Treatment seeking participants with Cocaine Use Disorder enrolled in a 12-week contingency management trial to reduce cocaine use. Participants were randomly assigned 1:1:1 to High Value Reinforcers (i.e., $55/negative urine sample) for cocaine abstinence (n = 41), Low Value Reinforcers (i.e., $13/negative urine sample) for cocaine abstinence (n = 33) or Non-Contingent Control (n = 33). Immune measures were collected at 6-week intervals. The High Value group had greatest use reductions, increased erythema and IL-6 and decreased IL-10 and CCL5, suggesting an activated immune response. Cocaine use reduction may promote changes in immune health.

本研究确定了减少可卡因使用对免疫功能的影响。患有可卡因使用障碍的求治者参加了为期 12 周的应急管理试验，以减少可卡因的使用。参与者按 1:1:1 的比例被随机分配到高价值强化物（即 55 美元/阴性尿样）以戒除可卡因（n = 41）、低价值强化物（即 13 美元/阴性尿样）以戒除可卡因（n = 33）或非权变控制（n = 33）。每隔 6 周收集一次免疫测定结果。高价值组的用量减少最多，红斑和 IL-6 增加，IL-10 和 CCL5 减少，表明免疫反应被激活。减少使用可卡因可能会促进免疫健康的变化。

引用次数: 0

Kidney injury: An overlooked manifestation in autoimmune encephalitis 肾损伤：自身免疫性脑炎中一个被忽视的表现

IF 2.9 4区医学 Q3 IMMUNOLOGY

Journal of neuroimmunology

Pub Date : 2024-10-28 DOI: 10.1016/j.jneuroim.2024.578472

Zhirong Fan , Jing Li , Yingchi Zhang , Juan Kang , Di Wang , Lijuan Liu , Min Li , Xiaodan Shi , Na Yuan , Yuanli Zhang , Fang Du , Wen Jiang

Aim

To investigate the prevalence and clinical features of kidney injury in patients with autoimmune encephalitis (AE).

Methods

Kidney injury was suspected in kidney-involving group due to persistent abnormal in urinary protein and serum albumin. Data on demographics and clinical features were compared between kidney-involving group and kidney-sparing group (patients without kidney injury) using Wilcoxon rank-sum test or chi-square test. Renal biopsy was conducted to identify the type of kidney injury.

Results

Approximate 30 % (32 of 108) patients with AE were suspicious of kidney injury. Nine patients further tested 24 h urine total protein, and seven of them had an elevated urine protein higher than 150 mg. The predominantly patterns of kidney injury were elevated urine protein, decreased serum albumin and normal kidney function. Compared to kidney-sparing group, the spectrum of AE antibodies in kidney-involving group was different, manifested as less anti-N-methyl-d-aspartate receptor antibodies (50 % vs. 72.4 %, p = 0.025) and more anti-contactin-associated protein like 2 antibodies (18.8 % vs. 1.3 %, p = 0.003). Definite pathological changes indicative of IgA nephropathy and membranous nephropathy in renal biopsy of two cases provided evidence of autoimmune attacks.

Discussion

Kidney injury occurred in considerable proportion of patients with AE. An in-depth screening for nephropathy could be essential for AE.

目的探讨自身免疫性脑炎（AE）患者肾损伤的发生率和临床特征。方法由于尿蛋白和血清白蛋白持续异常，怀疑肾损伤发生在累及肾脏组。采用Wilcoxon秩和检验或秩和检验比较肾脏受损组和肾脏未受损组的人口统计学和临床特征。结果约有 30% 的 AE 患者（108 例中有 32 例）怀疑有肾损伤。9 名患者进一步检测了 24 小时尿总蛋白，其中 7 人的尿蛋白升高超过 150 毫克。肾损伤的主要模式是尿蛋白升高、血清白蛋白降低和肾功能正常。与保肾组相比，累及肾脏组的 AE 抗体谱不同，表现为抗 N-甲基-d-天冬氨酸受体抗体较少（50% 对 72.4%，P = 0.025），而抗接触蛋白相关蛋白 2 抗体较多（18.8% 对 1.3%，P = 0.003）。两个病例的肾活检结果显示了 IgA 肾病和膜性肾病的明确病理改变，为自身免疫攻击提供了证据。深入筛查肾病对 AE 患者至关重要。

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引用次数: 0