Journal of neuroimmunology最新文献

{"title":"Retraction notice to “Chronic restraint stress promotes immune suppression through toll-like receptor 4-mediated phosphoinositide 3-kinase signaling” [Journal of Neuroimmunology 204 (2008) 13-19]","authors":"Yi Zhang , Ying Zhang , Junying Miao , Gregory Hanley , Charles Stuart , Xiuli Sun , Tingting Chen , Deling Yin","doi":"10.1016/j.jneuroim.2025.578710","DOIUrl":"10.1016/j.jneuroim.2025.578710","url":null,"abstract":"","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578710"},"PeriodicalIF":2.5,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144775673","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":"The immune response within Alzheimer's disease: from the lense of peripheral monocyte-derived macrophages","authors":"Hannah LeVasseur ,&nbsp;Beiyan Zhou","doi":"10.1016/j.jneuroim.2025.578711","DOIUrl":"10.1016/j.jneuroim.2025.578711","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is the most significant form of dementia characterized by neurodegeneration and higher-order cognitive decline affecting over 6.9 million Americans age 65 and older. Emerging evidence for AD pathogenesis has expanded mechanistic investigation from focusing on the central nervous system (CNS), to including the peripheral immune system. Microglia in CNS and their counterpart peripheral monocyte-derived macrophages (MDMs) share fundamental functions as innate cells that contribute to the inflammatory response, phagocytosis of debris, and tissue repair after injury. As recently recognized in AD pathogenesis, MDMs have distinct origins and respond differently to environmental cues relative to microglia, presenting unique potentials for therapeutic targeting outside of the blood-brain barrier. In this review, we will diverge from the previously highlighted primary immune regulator in the CNS, the microglia, to explore the significance of MDMs as a peripheral-origin contributor to the pathogenesis of AD.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578711"},"PeriodicalIF":2.5,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764135","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":"Ido1 or Ido2 deficiency in myeloid-derived cells attenuates TMEV-induced ictogenesis","authors":"Zoë A. MacDowell Kaswan ,&nbsp;Myrna Hurtado ,&nbsp;Emily Y. Chen ,&nbsp;Andrew J. Steelman ,&nbsp;Robert H. McCusker","doi":"10.1016/j.jneuroim.2025.578707","DOIUrl":"10.1016/j.jneuroim.2025.578707","url":null,"abstract":"<div><div>Viral encephalitis is a serious medical condition that causes neuroinflammation, neurodegeneration, cognitive deficits and seizures (ictogenesis), predisposing patients to epilepsy. In a preclinical setting, intracranial infection of C57BL/6 mice with Theiler's murine encephalomyelitis virus (TMEV) is the best-characterized animal model of viral encephalitis resulting in ictogenesis and temporal lobe epilepsy. Macrophages play a critical yet unclear role during encephalomyelitis: macrophage depletion reduces TMEV-induced ictogenesis, whereas prevention of macrophage infiltration into the brain reduces hippocampal damage without changing seizure incidence. Here, we explore the roles of indoleamine-2,3-dioxygenase (Ido) 1 and 2 from myeloid-derived cells (i.e. monocytes, macrophages and monocyte-derived dendritic cells) in the context of TMEV-induced ictogenesis and hippocampal gene expression. <em>Ido1</em> and <em>Ido2</em> gene expression is induced by inflammation. IDO1 and IDO2 proteins initiate the kynurenine pathway, by which tryptophan is converted into kynurenine but both proteins have poorly characterized non-enzymatic actions with unknown consequences during encephalomyelitis. In this study, we found that Ido1 and Ido2 deficiencies within myeloid-derived cells reduced ictogenesis without altering hippocampal inflammation-associated gene expression. In vitro infection of peritoneal macrophages demonstrated that genotype does not impact TMEV replication or cytokine expression, suggesting that the direct response of macrophages to infection is not the mechanism for the observed attenuation of ictogenesis in mice with myeloid Ido1 or Ido2 deficiencies.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578707"},"PeriodicalIF":2.5,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144860269","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":"Prolonged corticosteroid therapy and steroid-sparing maintenance immunotherapy lower relapse risk in pediatric and adult MOGAD","authors":"Yoji Hoshina ,&nbsp;Suzanne Liu ,&nbsp;Melissa A. Wright ,&nbsp;Alen Delic ,&nbsp;Ka-Ho Wong ,&nbsp;Robert Kadish ,&nbsp;Jonathan Galli ,&nbsp;John W. Rose ,&nbsp;John E. Greenlee ,&nbsp;M. Mateo Paz Soldán ,&nbsp;Julia Klein ,&nbsp;Lisa K. Peterson ,&nbsp;Tammy L. Smith ,&nbsp;Stacey L. Clardy","doi":"10.1016/j.jneuroim.2025.578709","DOIUrl":"10.1016/j.jneuroim.2025.578709","url":null,"abstract":"<div><h3>Background</h3><div>Most existing literature on predictors of myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) relapse predates the 2023 diagnostic criteria and have yielded mixed results. While prolonged corticosteroid use has been shown to reduce relapse rates in some studies, the optimal dose and duration remain unclear.</div></div><div><h3>Methods</h3><div>We conducted a retrospective study of patients treated for MOGAD at the University of Utah and Primary Children's Hospital who met the 2023 diagnostic criteria and either experienced a relapse or were followed for ≥12 months after the initial attack. A multivariable Andersen-Gill model assessed clinical and treatment factors associated with relapse risk. Corticosteroid doses were converted to prednisone equivalents, with duration defined by the period on ≥12.5 mg/day (≥0.16 mg/kg/day in pediatric patients).</div></div><div><h3>Results</h3><div>Seventy-two patients were included (median onset age 25.5 [IQR 11.75–46.5] years; of these, 47 [65.3 %] female; 30 [41.7 %] pediatric). Twenty-five (34.7 %) experienced at least one relapse. Optic neuritis was more common among adults (81 % vs. 56.7 %, <em>p</em> = 0.049), whereas acute disseminated encephalomyelitis was more frequent among pediatric patients (33.3 % vs. 2.4 %, <em>p</em> &lt; 0.001). Multivariable analysis showed that corticosteroids ≥12 weeks (HR 0.298, 95 % CI 0.1–0.887, <em>p</em> = 0.03) and maintenance immunotherapy (HR 0.061, 95 % CI 0.016–0.229, p &lt; 0.001) were associated with lower relapse risk. Sensitivity analysis showed that both rituximab (HR 0.099, 95 % CI 0.024–0.407, <em>p</em> = 0.001) and maintenance IVIg (HR 0.058, 95 % CI 0.007–0.471, <em>p</em> = 0.008) were independently associated with reduced relapse risk.</div></div><div><h3>Conclusion</h3><div>Prolonged corticosteroid therapy for ≥12 weeks and maintenance immunotherapy with rituximab or intravenous immunoglobulin independently lower relapse risk in MOGAD.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578709"},"PeriodicalIF":2.5,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767224","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":"Bridging the triad: A comprehensive review of Susac's syndrome","authors":"Alec Yakubik ,&nbsp;Elizabeth Delery","doi":"10.1016/j.jneuroim.2025.578708","DOIUrl":"10.1016/j.jneuroim.2025.578708","url":null,"abstract":"<div><div>Susac's Syndrome (SuS) is a rare, immune-mediated disorder characterized by encephalopathy, branch retinal artery occlusions (BRAO), and sensorineural hearing loss, with an estimated 450 diagnosed cases worldwide. Disease presentation varies in symptoms and duration, including vertigo, hearing loss, visual disturbances, migraine-like headaches, and central nervous system dysfunction. The current classification of SuS remains unclear due to a lack of pathophysiology and many hypotheses have been suggested, such as genetic predisposition and/or previous immune challenge causing SuS as a secondary disease. In this review, we present differential diagnoses and argue SuS's classification as a delayed-type hypersensitivity autoimmune disorder. Further familial genetic research is needed.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578708"},"PeriodicalIF":2.5,"publicationDate":"2025-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893279","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":"Neuroprotective effects of Analgecine by modifying cholesterol metabolism in EAE mice model of multiple sclerosis","authors":"Cuicui Yang ,&nbsp;Xinhai Jiang ,&nbsp;Zizhao Cheng ,&nbsp;Cengceng Zheng ,&nbsp;Chaoying Hu","doi":"10.1016/j.jneuroim.2025.578704","DOIUrl":"10.1016/j.jneuroim.2025.578704","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is a chronic autoimmune neurological disease characterized by inflammatory demyelination damage. Therapeutic alternatives for MS are still limited. Interventions to improve cholesterol homeostasis may be a viable approach to promoting the remyelination of MS patients. Analgecine (AGC), the extracts of Vaccinia-inoculated rabbit skin, is used in clinical for the treatment of low back pain. We previously found AGC had neuroprotective effect. In the present study, we aimed to discover the effect and mechanism of AGC on cholesterol homeostasis in a model of MS. In this study, we found that AGC effectively reduced the neurological deficit score and reversed the state of reduced body weight in the experimental autoimmune encephalomyelitis (EAE) mice. Furthermore, we also demonstrated that AGC treatment attenuated demyelination in the spinal cord and corpus callosum, amended loss of neurons in the hippocampal and cortical regions in EAE model. In addition, we identified the potential of AGC to well regulate cholesterol metabolism homeostasis by proteomic analysis, which may be related to its regulation of DHCR24 gene expression. Meanwhile, we also demonstrated in vitro and in vivo that AGC could effectively alleviate the abnormal cholesterol aggregation in microglia. Taken together, our study indicates that AGC is a promising potential agent for the treatment of MS by improving demyelination and neuron loss, which may be related to its ability in the regulation of cholesterol metabolism homeostasis.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578704"},"PeriodicalIF":2.5,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144757658","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":"SARS-CoV-2 spike antibody and T cell response in MS patients on high efficacy therapies post vaccine","authors":"Shrishti Saxena ,&nbsp;Alena Zhirova ,&nbsp;Rajesh Krishnan ,&nbsp;Brian Healy ,&nbsp;Eunnindy Sanon ,&nbsp;Niveditha Gopalakrishnan ,&nbsp;Alyssa Solberg ,&nbsp;Sarah Conway ,&nbsp;Tanuja Chitnis","doi":"10.1016/j.jneuroim.2025.578694","DOIUrl":"10.1016/j.jneuroim.2025.578694","url":null,"abstract":"<div><h3>Background</h3><div>There is limited knowledge about SARS-CoV-2 spike antibody and long-term T cell responses in multiple sclerosis (MS) patients on high efficacy treatments post SARS-CoV-2 vaccine.</div></div><div><h3>Objectives</h3><div>To assess spike antibody and T cell responses in MS patients on fingolimod (FIN), ocrelizumab (OCR) and healthy controls (HC) post vaccine.</div></div><div><h3>Methods</h3><div>We studied spike antibody seroconversion rates and T cell responses by flow cytometry in HC and MS patients.</div></div><div><h3>Results</h3><div>The seroconversion rate in FIN patients after 2-vax at 2-3 m 6/8 (75 %), 5-6 m 9/9 (100 %) and after 3 vax at 2-3 m 12/12 (100 %), 5-6 m 16/19 (84.21 %) and 8-12 m 5/5 (100 %). The seroconversion rate in OCR patients after 2-vax at 2-3 m 8/29 (27.6 %), 5-6 m 3/16 (18.8 %), 8-12 m 1/3 (33.3 %) and after 3 vax at 2-3 m 12/12 (100 %), 5-6 m 10/21 (47.6 %) and 8-12 m 7/12 (58.33 %). HC show a 100 % seroconversion rate. HC and OCR patients preserve both the percentage and absolute number of CD4+ T cells. FIN patients have a profound CD4+ T cell loss but compensatory rise in CD8+ T cell percentages. FIN patients exhibit the highest percentage of IFNγ+ CD4+ T cells and IFNγ+/TNFα+ CD8+ T cells.</div></div><div><h3>Conclusions</h3><div>Healthy controls show the highest spike antibody seroconversion rate while ocrelizumab treated patients remain low even after a third dose despite preserved CD4+ counts, whereas fingolimod treated patients lose CD4+ T cells but compensate with inflated CD8+ frequencies and a cytokine rich effector T cell profile.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578694"},"PeriodicalIF":2.5,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144739004","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":"Bergapten inhibiting NLRP3 inflammasome activation and pyroptosis to alleviate neuropathic pain in a rat mode of chronic constriction injury","authors":"Hai-Ping You,&nbsp;Li-Hong Zhang,&nbsp;He-Fan He,&nbsp;Zhi-Yuan Chen,&nbsp;Hong-Geng Wang,&nbsp;Wei-Feng Liu,&nbsp;Chong-Jun Xu","doi":"10.1016/j.jneuroim.2025.578706","DOIUrl":"10.1016/j.jneuroim.2025.578706","url":null,"abstract":"<div><div>Neuropathic pain is a persistent and treatment-resistant condition often linked to neuroinflammation and pyroptosis in the spinal cord. The NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome has emerged as a key contributor to this process. Here we investigate the efficacy of bergapten (5-Methoxypsoralen), a natural compound with anti-inflammatory activity, in managing neuropathic pain. A model of chronic constriction injury (CCI) was established in rats to induce neuropathic pain. Bergapten (100 mg/kg) was intraperitoneally administered once daily for 21 days. Mechanical and thermal pain sensitivity were evaluated at multiple time points. Spinal dorsal horn tissue was analyzed using immunofluorescence, western blot, and RT-qPCR. Bergapten significantly reduced thermal hyperalgesia and mechanical allodynia in CCI rats without affecting baseline nociception in sham controls. Molecular analyses showed decreased pyroptosis, reduced levels of cleaved caspase-1 and GSDMD-N, and suppressed expression of IL-6, IL-1β, and IL-18. Bergapten also downregulated NLRP3 and ASC and restored expression of miR-20b-5p. Bergapten alleviates neuropathic pain by inhibiting pyroptosis and neuroinflammation through suppression of the NLRP3 inflammasome pathway, suggesting its potential efficacy for treating neuropathic pain.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578706"},"PeriodicalIF":2.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144772784","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":"Beta adrenergic signaling as a therapeutic target for autoimmunity","authors":"Tatlock H. Lauten ,&nbsp;Emily C. Reed ,&nbsp;Tamara Natour ,&nbsp;Lauren J. Pitts ,&nbsp;Caroline N. Jojo ,&nbsp;Brooke L. Griffin ,&nbsp;Adam J. Case","doi":"10.1016/j.jneuroim.2025.578705","DOIUrl":"10.1016/j.jneuroim.2025.578705","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is an inflammatory demyelinating disorder of the central nervous system (CNS) characterized by an autoimmune response where both T-lymphocytes and proinflammatory interleukin 17A (IL-17A) are implicated in the pathogenesis of the disease. We recently identified a molecular mechanism involving beta-adrenergic 1 and 2 receptors (β1/2) in the polarization of T_H17 lymphocytes. Pharmacological and genetic inhibition of these receptors in combination, but not separately, impaired the ability of T-lymphocytes to produce IL-17A and instead promoted the differentiation of protective T_reg cells that secrete anti-inflammatory interleukin-10 (IL-10). However, it remained unclear whether this regulatory mechanism could serve as a novel therapeutic approach for autoimmune disorders mediated by IL-17A-producing T-lymphocytes, like MS. Using an animal model of MS, termed experimental autoimmune encephalomyelitis (EAE), we addressed the impact of beta adrenergic receptor blockade (genetically and pharmacologically) on EAE disease progression, severity, and T_H17/T_reg balance. Genetic deletion β1/2 receptors, either systemically or specifically on T-lymphocytes, significantly attenuated EAE disease severity and animal weight loss. Therapeutic pharmacological blockade of β1/2 receptors with either propranolol (lipophilic) or nadolol (aqueous) limited disease severity and weight loss similar to the genetic models, with combination therapy with anti-IL-17A antibodies showing the greatest disease remission. All models showed degrees of shifted T_H17/T_reg balance and decreased T-lymphocyte IL-17A production. Our data depict a novel role for β1/2 adrenergic signaling in the control of T_H17/T_reg cells in EAE, and provide new insight into the disease progression as well as offer a potential new pharmacological therapy for IL-17A-related autoimmune diseases.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578705"},"PeriodicalIF":2.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144713859","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":"Are corneal nerve and dendritic cell parameters assessed via corneal confocal microscopy good markers for multiple sclerosis? – A systematic review and meta-analysis","authors":"Prince K. Akowuah ,&nbsp;Esther Botchway ,&nbsp;Ebenezer Owusu ,&nbsp;Dominic A. Ohene ,&nbsp;Teresa Abonambugre ,&nbsp;Yusif Saeed Adam ,&nbsp;Phoebe Ahimah Asherow ,&nbsp;Berlinda E. Deletsu ,&nbsp;Jesse Doe ,&nbsp;Felicia Akyaa Akomeah ,&nbsp;David Totoe","doi":"10.1016/j.jneuroim.2025.578697","DOIUrl":"10.1016/j.jneuroim.2025.578697","url":null,"abstract":"<div><h3>Objective</h3><div>The current study evaluated corneal nerve and dendritic cell changes in multiple sclerosis (MS) compared to healthy controls.</div></div><div><h3>Methods</h3><div>The study was registered with PROSPERO (ID: CRD42024606762) and adhered to the PRISMA guidelines. PubMed, Scopus, and Web of Science databases were searched. Mean difference (MD), with a 95 % confidence interval, was used to assess outcomes. The quality of evidence was assessed using the GRADE system.</div></div><div><h3>Results</h3><div>12 cross-sectional comparative studies (<em>n</em> = 485 MS patients, <em>n</em> = 319 controls) met the inclusion criteria. Corneal nerve fiber density (MD = −8.35 fibers/mm², 95 % CI: −11.90 to −4.79; number of studies = 6), corneal nerve fiber length (MD = −4.05 mm/mm², 95 % CI: −5.74 to −2.36; number of studies = 9) and corneal nerve branch density (MD = −18.76 branches/mm², 95 % CI: −21.51 to −16.02; number of studies = 6) were significantly lower in MS compared to healthy controls. Heterogeneity was significant for corneal nerve fiber density and corneal nerve fiber length, but insignificant for corneal nerve branch density. No significant difference was found in corneal dendritic cell density; however, in the subgroup with disease duration ≤8 years, multiple sclerosis patients had significantly higher dendritic cell density (MD = 17.36 cells/mm², 95 % CI: 4.17 to 30.56; number of studies = 3).</div></div><div><h3>Conclusion</h3><div>Corneal nerve degeneration and dendritic cell changes assessment with corneal confocal microscopy may be an emerging tool with potential for disease monitoring. Further longitudinal studies are needed to validate these findings and clarify their correlation with MS progression and severity.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578697"},"PeriodicalIF":2.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144720922","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}