Journal of neuroimmunology最新文献

{"title":"Neoehrlichiosis in patients with multiple sclerosis in Halmstad, Sweden: A case series","authors":"Elias Ditlevsen Regen ,&nbsp;Daniel Victor ,&nbsp;Tijn Hendrikx","doi":"10.1016/j.jneuroim.2025.578787","DOIUrl":"10.1016/j.jneuroim.2025.578787","url":null,"abstract":"<div><div>Neoehrlichiosis is an emerging tick-borne infection. The documented cases of human infection demonstrate a varying symptomatology, diagnostic difficulties, a lacking clinical awareness of the condition and a considerable diagnostic delay. A high prevalence of the causative pathogen has been found in ticks in large parts of Europe, and there is believed to be a significant underdiagnosis. B-cell targeting therapy has been found a significant risk factor both for symptomatic and severe infection. However, the number of reports of neoehrlichiosis in multiple sclerosis (MS) patients is scarce, with only four documented cases to date. This case series portrays seven cases of neoehrlichiosis in six MS patients in southern Sweden, yielding a greater understanding of the infection in this patient group. The cases illustrate the elusive symptomatology of neoehrlichiosis, resulting in a diagnostic delay. The findings show that testing for neoehrlichiosis must be considered in patients with B-cell modifying therapy both in the case of fever, but also other suggestive symptoms, and disregarding season and recollection of tick bite. All patients were under active treatment with rituximab, but with significant differences in treatment duration, total accumulated dose and duration since last dose. No correlation was seen to decreased levels of immunoglobulin G (IgG), but rather to B-cell depletion. This illustrates the need to monitor CD19 and CD20 levels when assessing risk for neoehrlichiosis, and to consider screening for infection before onset of B-cell modifying therapy.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578787"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145445032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wash-out duration and lymphocyte count in switching from fingolimod to ofatumumab: A case report and literature review","authors":"Assunta Bianco ,&nbsp;Rosellina Russo ,&nbsp;Alessandra Cicia ,&nbsp;Sofia Marini ,&nbsp;Matteo Lucchini ,&nbsp;Massimiliano Mirabella","doi":"10.1016/j.jneuroim.2025.578808","DOIUrl":"10.1016/j.jneuroim.2025.578808","url":null,"abstract":"<div><div>Transitioning from sphingosine-1-phosphate modulators, such as fingolimod, to anti-CD20 therapies is common in patients with multiple sclerosis due to suboptimal disease control, progression, or family planning. However, the optimal washout period remains unclear, and cases of disease activity rebound following discontinuation of fingolimod have been documented. We present the case of a 43-year-old woman who developed severe rebound disease activity after transitioning from fingolimod to ofatumumab, despite a washout period of 28 days. The patient experienced a new lesion and neuropsychological impairment, which improved after treatment with high-dose methylprednisolone. Literature review highlights the complexity of factors influencing rebound, including washout duration, lymphocyte count, and disease control during fingolimod therapy. Evidence suggests that initiating ofatumumab treatment without a prolonged washout period may mitigate rebound risk.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578808"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145615382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurosarcoidosis masquerading as recurrent tumefactive demyelinating-appearing brain lesions: An 8-year diagnostic odyssey","authors":"Nirmalya Ray ,&nbsp;Russoti Das ,&nbsp;Mithun Sekhar ,&nbsp;Debraj Jash ,&nbsp;Shramana Deb ,&nbsp;Ritwick Mondal ,&nbsp;Jayanta Roy ,&nbsp;Julián Benito-León","doi":"10.1016/j.jneuroim.2025.578802","DOIUrl":"10.1016/j.jneuroim.2025.578802","url":null,"abstract":"<div><h3>Background</h3><div>Neurosarcoidosis is a rare inflammatory condition that can occasionally present with recurrent tumefactive lesions resembling those of idiopathic demyelinating diseases. Diagnosis is frequently delayed because clinical and radiological features overlap with demyelinating disorders, and systemic signs may initially be absent.</div></div><div><h3>Case presentation</h3><div>We report a woman who first presented at 23 years of age with a tumefactive demyelinating-appearing brain lesion and, eight years later, experienced recurrence with new involvement of the brain and spinal cord. The second episode featured a new tumefactive demyelinating-appearing brain lesion, longitudinally extensive transverse myelitis, vertebral enhancement, and systemic manifestations. Imaging revealed mediastinal lymphadenopathy and multiple hypodense lesions in the liver and spleen, while histopathologic examination of a mediastinal lymph node demonstrated noncaseating granulomas, confirming sarcoidosis.</div></div><div><h3>Conclusion</h3><div>To our knowledge, this is the first detailed report of neurosarcoidosis evolving from an initially isolated tumefactive demyelinating-appearing brain lesion to a later episode characterized by recurrent brain involvement with simultaneous spinal and systemic disease after a prolonged asymptomatic interval. Clinicians should consider neurosarcoidosis in the differential diagnosis of tumefactive demyelinating-appearing brain lesions, particularly when an initially isolated presentation is followed by subsequent brain, spinal, and systemic involvement, even in young patients without systemic features at onset.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578802"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145495885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetically reduced MTHFR activity confers protection against multiple sclerosis","authors":"Iyas Daghlas ,&nbsp;John V. Pluvinage ,&nbsp;Dipender Gill","doi":"10.1016/j.jneuroim.2025.578784","DOIUrl":"10.1016/j.jneuroim.2025.578784","url":null,"abstract":"<div><h3>Objectives</h3><div>Methylenetetrahydrofolate reductase (MTHFR) generates the active form of folate required for homocysteine metabolism. The C677T variant in <em>MTHFR</em> reduces enzymatic activity, increases homocysteine levels, and is associated with risk of several neurological diseases. However, its link to multiple sclerosis (MS) risk remains uncertain. We therefore investigated the association of this variant with risk and severity of MS.</div></div><div><h3>Methods</h3><div>We obtained genetic associations of C677T with homocysteine levels (<em>n</em> = 1210), MS risk (meta-analysis of three datasets: 43,069 cases), and MS severity (12,584 cases). We report associations of the C677T variant with MS risk and severity, and performed sensitivity analyses to assess genetic confounding.</div></div><div><h3>Results</h3><div>There was strong statistical evidence for an association of the C677T variant with risk of MS (pooled odds ratio [OR] of MS per homocysteine-raising allele 0.91, 95 % confidence interval [CI] 0.89–0.93, <em>P</em> = 7.59 × 10⁻¹⁴). The OR when scaled to an SD increase in genetically determined homocysteine levels due to MTHFR perturbation was 0.73 (95 % CI 0.66–0.79, <em>P</em> = 7.27 × 10⁻¹⁴). Colocalization analyses supported C677T as a shared causal variant for MS and homocysteine levels at the <em>MTHFR</em> locus. By contrast, no association was found between C677T and MS severity (<em>P</em> = 0.92).</div></div><div><h3>Discussion</h3><div>These results support a novel biological hypothesis linking impaired MTHFR function to protection from MS. Further research is needed to elucidate the underlying mechanism and explore potential therapeutic implications.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578784"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145419761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Neuroimmunological Axis between systemic autoimmunity and Parkinson's disease following long-COVID: A case series","authors":"Esra Demir Unal","doi":"10.1016/j.jneuroim.2025.578795","DOIUrl":"10.1016/j.jneuroim.2025.578795","url":null,"abstract":"<div><h3>Background</h3><div>Long COVID, a multisystemic syndrome following SARS-CoV-2 infection characterized by persistent immune dysregulation, systemic inflammation, and neuroimmune dysfunction, is a significant area of investigation in the neurological sciences. The hypothesis that this pathophysiological state can trigger de novo autoimmune diseases and potentially accelerate underlying neurodegenerative processes is gaining traction. This case series aims to illuminate the potential neuroimmunological link between these conditions by presenting the patients who developed de novo Crohn's disease (CD) and ankylosing spondylitis (AS) following Long COVID and were subsequently diagnosed with post-COVID Parkinson's Disease (PD).</div></div><div><h3>Case presentations</h3><div>The first case is a 50-year-old female who developed de novo CD six months after COVID-19 pneumonia, managed with the TNF-α inhibitor. Eighteen months later, she presented with parkinsonian motor deficits. The post-COVID PD diagnosis was supported by susceptibility-weighted MRI showing loss of nigrosome-1 and DAT-SPECT revealing a presynaptic dopaminergic deficit. The second case is a 48-year-old female who was diagnosed with de novo AS eight months post-COVID, treated with adalimumab. Twenty-six months later, she developed progressive bradykinesia and rigidity. Neuroimaging confirmed post-COVID PD with corresponding loss of nigrosome-1 and a presynaptic dopaminergic deficit on DAT-SPECT. In both genetically negative cases, dopaminergic therapy led to substantial motor improvement, with Unified Parkinson's Disease Rating Scale (UPDRS) Part IIIscores decreasing from 8 to 3 and 14 to 4, respectively.</div></div><div><h3>Conclusion</h3><div>This case series proposes a pathogenic cascade wherein SARS-CoV-2 infection acts as an environmental trigger, initiating a Long COVID-associated immune dysregulation that first precipitates a systemic autoimmune disorder. We hypothesize that this sustained inflammatory milieu subsequently accelerates the dysfunction of the dopaminergic system in predisposed individuals, thereby unmasking the clinical phenotype of post-COVID PD. This novel association highlights a potential nexus between virally-induced autoimmunity and subsequent neurodegeneration, offering a new perspective in the field of neuroimmunology.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578795"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145445029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurological adverse events of immune checkpoint inhibitors: A practical guide to diagnosis with a focus on neuroimaging findings","authors":"Simone Rossi ,&nbsp;Alberto Vogrig ,&nbsp;Laura Fionda ,&nbsp;Valentina Damato ,&nbsp;Luca Spinardi ,&nbsp;Maria Guarino","doi":"10.1016/j.jneuroim.2025.578816","DOIUrl":"10.1016/j.jneuroim.2025.578816","url":null,"abstract":"<div><div>The use of immune checkpoint inhibitors (ICIs), a class of oncologic therapies that enhance anti-tumor immunity, may be complicated by the occurrence of neurologic immune-related adverse events (n-irAEs). ICI-induced neurotoxicities predominantly affect the peripheral nervous system, manifesting as myositis, polyradiculoneuropathies and cranial neuropathies and, less frequently, involve the central nervous system, typically as encephalitis or myelitis. The diagnosis of n-irAEs relies on the exclusion of alternative etiologies – such as cancer dissemination, chemotherapy-induced neurotoxicities, and neuroinfections – and the recognition of specific clinical syndromes.</div><div>Neuroradiological investigations, particularly magnetic resonance imaging (MRI), play a crucial role in ruling out differential diagnosis, mainly cancer dissemination. Furthermore, MRI can support the clinical suspicious of an immune-mediated process by demonstrating indirect signs of neuroinflammation, including tissue edema and gadolinium enhancement. Nuclear medicine techniques, such as position emission tomography and scintigraphy, may also aid in the assessment of ICI-induced encephalitis and parkinsonism.</div><div>Despite the recognized clinical relevance of imaging investigations in the diagnosis of n-irAEs, a detailed characterization of neuroradiological features of ICI-induced neurotoxicities remains limited. In this Review, we provide a comprehensive description of the imaging findings associated with n-irAEs and summarize the diagnostic work-up of these challenging disorders, emphasizing the central role of neuroimaging in their evaluation.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578816"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145615380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wearable-based physiological monitoring and brain magnetic resonance imaging metrics in multiple sclerosis: A feasibility study","authors":"Yusei Miyazaki ,&nbsp;Hiroaki Yokote ,&nbsp;Juichi Fujimori ,&nbsp;Kenzo Sakurai ,&nbsp;Akifumi Hagiwara ,&nbsp;Satoshi Fujino ,&nbsp;Toshikazu Fukami ,&nbsp;Eri Takahashi ,&nbsp;Mai Miyagishi ,&nbsp;Megumi Uwatoko ,&nbsp;Yoko Sugimura ,&nbsp;Itaru Amino ,&nbsp;Sachiko Akimoto ,&nbsp;Keisuke Izumi ,&nbsp;Kazumichi Minato ,&nbsp;Naoya Minami ,&nbsp;Masaaki Niino","doi":"10.1016/j.jneuroim.2025.578819","DOIUrl":"10.1016/j.jneuroim.2025.578819","url":null,"abstract":"<div><h3><strong>Background</strong></h3><div>Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Physiological monitoring may be useful for monitoring the progression of MS and its underlying neurodegenerative processes</div></div><div><h3><strong>Objective</strong></h3><div>This cross-sectional study evaluated the feasibility of assessing associations of physiological parameters measured by a wearable sensor with CNS atrophy and lesion burden in individuals with MS.</div></div><div><h3><strong>Methods</strong></h3><div>Thirty MS patients (relapsing-remitting [<em>n</em> = 23], secondary progressive [<em>n</em> = 5], primary progressive [n = 2]) were monitored using a wrist-worn sensor (Fitbit inspire 3) for up to 30 days, and 29 physiological parameters were obtained. Global and regional brain volumes, T2 lesion volume (T2LV), and C2/3 cervical spinal cord cross-sectional area (C2/3 CSA) were analyzed based on brain MRI. Associations between sensor-derived parameters and neuroimaging measures were assessed using correlation analyses adjusted for age and gender</div></div><div><h3><strong>Results</strong></h3><div>The proportion of deep sleep was associated with T2LV (partial spearman's ρ [ρ_partial] = −0.46, 95 % confidence interval [−0.74, −0.04]) and C2/3 CSA (ρ_partial = 0.59 [0.32, 0.76]). The coefficient of variation of RR intervals during sleep was associated with normalized brain volume (ρ_partial = 0.41 [0.00, 0.74]). The minimum (ρ_partial = −0.44 [−0.72, −0.04]) and range of heart rate (ρ_partial = 0.41 [0.08, 0.68]) during daytime, step counts (ρ_partial = 0.64 [0.40, 0.82]), and total metabolic equivalents (ρ_partial = 0.54 [0.18, 0.79]) were associated with C2/3 CSA</div></div><div><h3><strong>Conclusion</strong></h3><div>The findings suggest the feasibility of using wearable sensors to detect physiological parameters reflective of neuropathology in patients with MS.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578819"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145615379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prior dexamethasone exposure attenuates the therapeutic efficacy of mouse bone marrow-derived mesenchymal stem cells in experimental autoimmune encephalomyelitis by fostering a hostile immunological microenvironment","authors":"Yaling Zhang ,&nbsp;Xiaoqiang Lv ,&nbsp;Qing Wang ,&nbsp;Xuan Ma ,&nbsp;Ruotong Wu ,&nbsp;Tingting Cui ,&nbsp;Xiaoli Ding ,&nbsp;Qian Zhang ,&nbsp;Luting Yang ,&nbsp;Cungen Ma ,&nbsp;Yaping Yan","doi":"10.1016/j.jneuroim.2025.578814","DOIUrl":"10.1016/j.jneuroim.2025.578814","url":null,"abstract":"<div><div>Bone marrow-derived mesenchymal stem cells (BMSCs) are promising candidates for treating autoimmune diseases like multiple sclerosis (MS) due to their ability to differentiate into multiple lineages and their immunomodulatory properties. However, the immunomodulatory capacity of BMSCs is highly adaptable, and primarily regulated by inflammatory factors. In this study, we evaluated the therapeutic effectiveness of BMSCs in dexamethasone (DEX)-pretreated experimental autoimmune encephalomyelitis (EAE) mice. Our results demonstrated a significant interaction between DEX and BMSCs. In contrast to their effect in non-pretreated mice, BMSCs administration in DEX-pretreated EAE mice resulted in a significant increase in infiltrating CD4⁺ T cells and a concomitant decrease in regulatory T (Treg) cell populations in the central nerves system, which likely resulted from DEX-induced changes in the peripheral immune microenvironment. Our findings in the EAE model indicate that the immune microenvironment established by DEX pretreatment is detrimental to the efficacy of BMSC therapy. This preclinical evidence suggests that evaluating the peripheral immune status may be a critical consideration for future clinical studies of MSC treatment in MS.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578814"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145604673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exogenous IL-33 mitigates inflammatory responses by suppressing the NF-Κb signaling pathway, promoting blood-spinal cord barrier repair and neural functional recovery","authors":"Minghao Xie ,&nbsp;Yuhang Diao ,&nbsp;Jing Zhang ,&nbsp;Mingyu Hao ,&nbsp;Zhitan Wang ,&nbsp;Rui Tan ,&nbsp;Jing Ma ,&nbsp;Xiaojun Hu ,&nbsp;Zhenghao Hao ,&nbsp;Tao Zhu","doi":"10.1016/j.jneuroim.2025.578800","DOIUrl":"10.1016/j.jneuroim.2025.578800","url":null,"abstract":"<div><h3>Background</h3><div>Neuroinflammation following spinal cord injury (SCI) is a critical contributor to secondary damage. This inflammatory response disrupts the integrity of the blood-spinal cord barrier (BSCB), leading to neural tissue edema and impaired neural function. Interleukin-33 (IL-33), a tissue-derived cytokine belonging to the IL-1 family, is detectable in both tissues and blood following neural injury. While the neuroprotective effects of exogenous IL-33 have been demonstrated in models of traumatic brain injury (TBI) and epilepsy, its role in spinal cord injury remains unexplored. Therefore, this study employs a mouse spinal cord contusion model to investigate the potential role of exogenous IL-33 in BSCB repair.</div></div><div><h3>Methods</h3><div>We established a spinal cord contusion model in mice and administered exogenous IL-33 via intraperitoneal injection to investigate its mechanisms in neural repair. Behavioral assessments were conducted on days 1, 3, 7, and 14 post-SCI, revealing the effects of IL-33 on long-term neural function. Additionally, immunofluorescence staining, Western blotting, ELISA, Evans blue leakage assays, TUNEL staining, hematoxylin-eosin (HE) staining, and Nissl staining were performed on day 3 or 7 post-SCI to evaluate the impact of IL-33 on neuroinflammation, BSCB integrity, and neuronal apoptosis.</div></div><div><h3>Results</h3><div>We found that exogenous IL-33 significantly promoted neural functional recovery in SCI mice, with particularly pronounced effects observed after 7 days. Subsequent analysis confirmed that IL-33 was primarily expressed in the nuclei of astrocytes following SCI and exhibited high expression levels in the spinal cord of SCI mice. Exogenous IL-33 modulated the NF-κB signaling pathway, suppressing the expression of downstream pro-inflammatory cytokines. Additionally, IL-33 inhibited microglial activation and facilitated their polarization toward an anti-inflammatory phenotype, thereby mitigating spinal cord inflammation.Furthermore, the administration of recombinant IL-33 increased the expression of tight junction proteins, including ZO-1, Occludin, and Claudin-5. These changes contributed to BSCB repair, reducing spinal cord edema and improving neurological recovery in mice. Lastly, IL-33 demonstrated a protective effect against neuronal apoptosis, further underscoring its neuroprotective potential.</div></div><div><h3>Concusion</h3><div>In summary, we demonstrated the anti-inflammatory and anti-apoptotic effects of exogenous IL-33, elucidating its underlying mechanisms. Notably, we identified its role in promoting BSCB repair for the first time. These findings support the potential use of exogenous IL-33 as a therapeutic strategy for early intervention in spinal cord injury.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578800"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145468396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory ratios as early predictors of disease severity and immunotherapy response in autoimmune encephalitis","authors":"Mingxing Yu ,&nbsp;Nana Zhang ,&nbsp;Chunyan Chen,&nbsp;Yuxuan He,&nbsp;Jing Meng,&nbsp;Wen Luo,&nbsp;Yi Liang,&nbsp;Yi Guo,&nbsp;Liang Yu","doi":"10.1016/j.jneuroim.2025.578786","DOIUrl":"10.1016/j.jneuroim.2025.578786","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to evaluate and compare the predictive value of systemic inflammatory ratios—including the neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic inflammation index (SII), and C-reactive protein (CRP)—for disease severity, immunotherapy response, and in-hospital mortality in patients with autoimmune encephalitis (AE).</div></div><div><h3>Methods</h3><div>A total of 389 AE patients diagnosed between December 2014 and January 2024 were retrospectively enrolled. Demographic, clinical, and laboratory data were collected. Inflammatory markers were measured prior to immunotherapy. Patients were stratified based on ICU admission and treatment response. Receiver operating characteristic (ROC) curves were used to assess the predictive performance of each biomarker.</div></div><div><h3>Results</h3><div>ICU-admitted patients (<em>n</em> = 86) exhibited significantly higher NLR, PLR, SII, and CRP levels compared to non-ICU patients (all <em>p</em> &lt; 0.05). NLR showed the highest predictive accuracy for ICU admission (AUC = 0.786). Combined NLR and CRP further improved prediction (AUC = 0.804). For immunotherapy response, NLR and PLR were significantly elevated in poor responders (<em>p</em> &lt; 0.05), with PLR demonstrating an AUC of 0.728. Regarding mortality, PLR and SII were the strongest predictors (AUC = 0.850 and 0.799, respectively), and their combination achieved an AUC of 0.856.</div></div><div><h3>Conclusion</h3><div>Inflammatory ratios, particularly NLR and PLR, serve as accessible and reliable biomarkers for predicting critical illness, treatment response, and mortality in AE patients. Their integration into clinical practice may facilitate early risk stratification and personalized treatment strategies.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"410 ","pages":"Article 578786"},"PeriodicalIF":2.5,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145401228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}