Journal of neuroimmunology最新文献

{"title":"Before assuming the association of plasma interleukin thirty-three (IL-33) levels with aggression in schizophrenia, all other causes of psychosis should be discarded","authors":"João Gama-Marques , Josef Finsterer","doi":"10.1016/j.jneuroim.2025.578729","DOIUrl":"10.1016/j.jneuroim.2025.578729","url":null,"abstract":"","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578729"},"PeriodicalIF":2.5,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879113","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":"Immunostimulatory and immunomodulatory effects of duloxetine and venlafaxine on p38 MAPK and PI3K pathways","authors":"Esra Aydemir ,&nbsp;Derya Yetkin ,&nbsp;Furkan Ayaz","doi":"10.1016/j.jneuroim.2025.578728","DOIUrl":"10.1016/j.jneuroim.2025.578728","url":null,"abstract":"<div><div>Anti-depressants have been used more widely throughout the world. Their mood altering activities are appreciated but determining their side effects or possible effects on the immune system is crucial. In our study, we focused on two prominent drugs that have been used against anxiety and depression. Serotonin and norepinephrine reuptake inhibitor (SNRI) anti-depressants Duloxetine and Venlafaxine were tested <em>in vitro</em> on the mammalian macrophages. Their immunostimulatory (inflammatory potential) activities were tested on inactivated macrophages whereas their immunomodulatory, possible anti-inflammatory activities were tested on the LPS activated macrophages. The production levels of pro-inflammatory cytokines were measured by ELISA. The levels of phosphorylated (active) p38 MAPK and PI3K proteins were determined by flow cytometry analysis and their possible intracellular mechanisms of action were demonstrated. According to our results, these drugs had differential effects on the macrophages. Duloxetine triggered a mild inflammatory response in the unactivated macrophages whereas; it had anti-inflammatory effects on already activated macrophages. Venlafaxine lacked this immunostimulatory activity on unactivated macrophages and had mild anti-inflammatory activities on the activated macrophages. These results suggest that these drugs can be differentially utilized against patients with inflammatory problems (Duloxetine) and patients without inflammatory problems (Venlafaxine).</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578728"},"PeriodicalIF":2.5,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144866561","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":"Inhibition of astrocytic toll-like receptor 4 contributes to sevoflurane pretreatment-induced anti-neuroinflammation following focal cerebral ischemia","authors":"You-Liang Deng ,&nbsp;Shi-Bin Du ,&nbsp;Guo-Qing Cao ,&nbsp;Xiang-Rui Li ,&nbsp;Jing-Yun Wang ,&nbsp;Ling-Wu ,&nbsp;Guo-Yun Lin ,&nbsp;Zhuo-Xi Wu ,&nbsp;Hong Li","doi":"10.1016/j.jneuroim.2025.578720","DOIUrl":"10.1016/j.jneuroim.2025.578720","url":null,"abstract":"<div><h3>Background</h3><div>Sevoflurane, a widely used clinical anesthetic, exhibits neuroproctive properties though its precise mechanisms remain unclear. Astrocytes, a critical regulators of immune responses, actively participate in sevoflurane-mediated neuroprotection against ischemia. Toll-like receptor 4 (TLR4), a key molecule for conversion from pro-inflammatory astrocytes to anti-inflammatory astrocytes phenotypes. The present study explores the role of astrocytic TLR4 in sevoflurane preconditioning mediated neuroprotection after focal cerebral ischemia.</div></div><div><h3>Methods</h3><div>In vivo, mice were preconditioned with 2.0 % sevoflurane before right middle cerebral artery occlusion/reperfusion (MCAO/R). In vitro, primary astrocytes were pretreated with sevoflurane and followed by 4 h oxygen-glucose deprivation for astrocytes and 2 h for astrocyte-neuron cocultures. Astrocytic TLR4 expression and its role in sevoflurane preconditioning in cerebral ischemia were assessed using western blotting, enzyme-linked immunosorbent assay (ELISA) and flow cytometry.</div></div><div><h3>Results</h3><div>The expression of TLR4 and the levels of inflammatory cytokines both within the penumbra and in primary astrocytes significantly increased following ischemia, further exacerbating neural damage. In vivo, sevoflurane preconditioning reduced the expression of TLR4 as well as the levels of TNFα and IL-6. Consistently, it improved neurological deficit scores and decreased infarct volume. In vitro, sevoflurane preconditioning prevented the increasing of TLR4 as well as the levels of TNFα and IL-6 of primary astrocytes and decreased the over-expression of cleaved-caspase 3 and primary neuron apoptosis in astrocyte-neuron co-cultures.</div></div><div><h3>Conclusions</h3><div>Our findings demonstrate that sevoflurane preconditioning attenuates ischemia-mediated neuroinflammation by suppressing astrocytic TLR4 expression, highlighting its therapeutic potential against neuroinflammation induced by focal cerebral ischemia.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578720"},"PeriodicalIF":2.5,"publicationDate":"2025-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144889966","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":"Association of interleukins 17A and 22 levels and their common genetic polymorphisms in Guillain Barré syndrome","authors":"Afifa Iqbal ,&nbsp;Bushra Mubarak ,&nbsp;Ali Amar ,&nbsp;Shahid Mukhtar ,&nbsp;Saba Khaliq ,&nbsp;Romeeza Tahir","doi":"10.1016/j.jneuroim.2025.578721","DOIUrl":"10.1016/j.jneuroim.2025.578721","url":null,"abstract":"<div><h3>Background</h3><div>Guillain-Barré syndrome (GBS) is an autoimmune and multifactorial disorder. Its immunopathogenesis involves activation of the aberrant Th17 pathway. Serum levels of Th17-associated cytokines (IL-17A and IL-22) and their genetic variants were compared between GBS patients and healthy controls.</div></div><div><h3>Subjects and methods</h3><div>Forty clinically diagnosed acute-phase patients with GBS and 40 healthy controls of Pakistani origin were included. Serum IL-17A and IL-22 levels were determined by ELISA. IL-22 and IL-17A gene variants were genotyped using PCR-RFLP and confirmed by Sanger sequencing. Functional significance analyses of both SNPs were performed using two modern databases: RegulomeDB version 2.2, and GTEx version 10. Data was analyzed using SPSS version 24, SNPatats, Vassarstats odds ratio calculator, and GraphPad Prism software.</div></div><div><h3>Results</h3><div>Mean ± SD age of GBS patients was more (42.03 ± 11.2 years) than control group (37.5 ± 12.1 years) (<em>p</em>-value = 0.09). Male to female ratio was 2.3:1. Serum levels of IL-17A and IL-22 were higher in GBS patients than in healthy controls (<em>p</em> &lt; 0.0001). For IL-22 rs2227485, the presence of variant alleles in homozygous (A/A) and heterozygous (G/A) alleles was strongly associated with susceptibility to GBS (ORs = 13.17 and 5.73, respectively, <em>p</em> = 0.0001). IL-17A rs3748067 SNP did not show a statistically significant association with GBS. The presence of the variant allele of the IL-22 SNP was associated with increased levels of cytokines in a dose-dependent manner (<em>p</em> &lt; 0.0001).</div></div><div><h3>Conclusion</h3><div>IL-17A and IL-22 play important roles in the pathogenesis of GBS. Serum IL-17 and IL-22 cytokines, along with their genetic variants, are aberrant in GBS patients.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578721"},"PeriodicalIF":2.5,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879112","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":"Neurotoxicity associated with chimeric antigen receptor T-cell therapy","authors":"Miriam Wronski ,&nbsp;Robb Wesselingh ,&nbsp;Christina Kazzi ,&nbsp;Nabil Seery ,&nbsp;Katherine Ko ,&nbsp;Jian Li ,&nbsp;Tracie H. Tan ,&nbsp;Ty Simpson ,&nbsp;Cassandra Abbott ,&nbsp;Shaun Fleming ,&nbsp;Shafqat Inam ,&nbsp;Constantine S. Tam ,&nbsp;Shu Min Wong ,&nbsp;Terence O'Brien ,&nbsp;Anneke van der Walt ,&nbsp;Andrew Spencer ,&nbsp;Helmut Butzkueven ,&nbsp;Mastura Monif","doi":"10.1016/j.jneuroim.2025.578717","DOIUrl":"10.1016/j.jneuroim.2025.578717","url":null,"abstract":"<div><div>Chimeric antigen receptor T cell (CAR-T) therapy involves reengineering patient-derived or donor-derived T cells to express a synthetic CAR that can recognise specific cell-surface antigens, independently of major histocompatibility complex molecules. As of March 2025, six autologous CAR-T cell products have received regulatory approval from the United States Food and Drug Administration (FDA) for B-cell derived haematological malignancies and multiple myeloma, delivering effective and durable treatment responses. All currently approved CAR-T cell therapy products target either CD19 or B-cell maturation antigen (BCMA). However, there is an expansive list of new CAR-T constructs and/or indications currently being explored in the pre-clinical stages and clinical trials.</div><div>Although the therapeutic potential of CAR-T cell therapy is substantial, the more widespread application of CAR-T cell therapy faces challenges, including overcoming unique and clinically significant CAR-T therapy-associated toxicities, namely cytokine release syndrome (CRS) and immune-effector cell associated neurotoxicity syndrome (ICANS). CAR-T cell-associated neurotoxicity can present with a diverse range of neurological and cognitive symptoms and signs, including tremor, dysgraphia, cognitive dysfunction, aphasia, seizures, and rarely cerebral oedema and death. As new CAR-T constructs and indications enter the therapeutic landscape, new class-specific toxicities have also emerged, including delayed-onset neurotoxicity with features of parkinsonism, as seen with BCMA-directed therapies in the pivotal clinical trials for multiple myeloma.</div><div>Whilst much progress has been made in understanding CRS, comprehensive information about the clinical, biological and radiological correlates of CAR-T cell-associated neurotoxicity, and its mechanistic underpinnings remain largely unknown. Furthermore, prophylactic or pre-emptive intervention strategies have been hindered by the lack of predictive or diagnostic biomarkers for ICANS. Considering the lack of targeted therapies for ICANS, detailed analysis of the associated biomarkers remains a key area of unmet need in the field. This review provides a detailed analysis of CAR-T cell-associated neurotoxicity, with a focus on the novel pathophysiological insights into disease mechanisms, the clinical manifestations and diagnostic evaluation, candidate biomarkers for neurotoxicity, and the current therapeutic landscape for ICANS management.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578717"},"PeriodicalIF":2.5,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144830039","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":"Clinical utility of autoantibodies in the diagnosis and management of Myasthenia gravis","authors":"Shadi El-Wahsh ,&nbsp;Sudarshini Ramanathan ,&nbsp;Stephen Reddel","doi":"10.1016/j.jneuroim.2025.578718","DOIUrl":"10.1016/j.jneuroim.2025.578718","url":null,"abstract":"<div><div>Myasthenia gravis is an autoimmune neuromuscular disease characterised by fatigable muscle weakness. The disease is caused by autoantibodies targeting components of the post-synaptic neuromuscular junction, which are identifiable in 90 % of cases. The most well-known and best-characterised of these is acetylcholine-receptor (AChR) antibody, which is present in approximately 50 % of ocular and 85 % of generalised MG patients. Other recognised pathogenic autoantibodies in MG target muscle specific kinase (MuSK) and low-density lipoprotein-receptor related protein 4 (LRP4), present in approximately 5–10 % and 1–5 % of MG cases respectively. Some autoantibodies are not directly pathogenic but inform disease severity and thymic status. Many other autoantibodies are described in MG, although their pathogenic role and clinical significance is yet to be determined. These include autoantibodies targeting COLQ, cortactin, rapsyn, AChE, and Kv1.4. In this review, we discuss the clinical utility of all autoantibodies implicated in MG to date, including their role in the diagnosis, management, and monitoring of the disease.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578718"},"PeriodicalIF":2.5,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826319","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":"sTREM2 as a mediator in the association between life-threatening events and depression","authors":"Alejandro Olaviaga ,&nbsp;Leandro Nicolás Grendas ,&nbsp;Luciana Carla Chiapella ,&nbsp;Romina Isabel Álvarez Casiani ,&nbsp;Ángeles Romina Arena ,&nbsp;Vera Tifner ,&nbsp;Cintia Romina Prokopez ,&nbsp;Eugenio Antonio Carrera Silva ,&nbsp;Andrea Emilse Errasti ,&nbsp;Federico Manuel Daray","doi":"10.1016/j.jneuroim.2025.578719","DOIUrl":"10.1016/j.jneuroim.2025.578719","url":null,"abstract":"<div><h3>Background</h3><div>Depression is a highly prevalent and disabling condition, affecting approximately 280 million people globally. Emerging evidence points to a significant role of neuroinflammation in the pathophysiology of depression. The soluble triggering receptor expressed on myeloid cells-2 (sTREM2) has been identified as a potential marker of neuroinflammation.</div></div><div><h3>Objective</h3><div>This study aims to investigate the potential mediating role of sTREM2 in the relationship between perceived stress, measured by the List of Threatening Events, and current depressive symptoms in patients with major depressive episodes (MDE).</div></div><div><h3>Methods</h3><div>This secondary analysis was conducted on data from a multicenter, case-control study of participants with current MDE (<em>n</em> = 39) and healthy controls (HC, <em>n</em> = 42). Plasma sTREM2 levels were measured using bead-based multiplex assays. Depression was assessed using the Hamilton Depression Rating Scale (HDRS-17) and Life-Threatening Events (LTE) were quantified with the Stressful Life Events Scale. A mediation analysis was conducted to explore the role of sTREM2 in the relationship between depression and LTE.</div></div><div><h3>Results</h3><div>Patients with current MDE exhibited higher plasma sTREM2 levels compared to HC (<em>p</em> = 0.006). Recent stress was positively associated with sTREM2 (<em>p</em> = 0.032), and both LTE scores and sTREM2 levels were significant predictors of current MDE (<em>p</em> = 0.009, <em>p</em> = 0.035). Mediation analysis showed that sTREM2 accounted for 17 % of the relationship between recent stress and depression (<em>p</em> = 0.028).</div></div><div><h3>Conclusion</h3><div>Our findings suggest that sTREM2 may play a mediating role in the link between stress and depression, highlighting neuroinflammation as a potential pathway in the development of depression.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578719"},"PeriodicalIF":2.5,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826351","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":"Immunity in Parkinson's disease – The role of innate responses","authors":"A.R. Satvik Iyengar ,&nbsp;Peter R. Dunkley,&nbsp;Phillip W. Dickson","doi":"10.1016/j.jneuroim.2025.578716","DOIUrl":"10.1016/j.jneuroim.2025.578716","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a debilitating neurodegenerative disorder that is characterized by motor dysfunction and deterioration of quality of life. PD is caused by a selective degeneration of the dopaminergic neurons in the substantia nigra region of the mid brain. Although, centuries have passed since the identification of PD, the exact pathogenic mechanism of PD is yet to be defined. It is understood that PD is a multifactorial disease that involves several cellular processes including immunological dysfunction. This review provides a brief introduction to PD and the innate immune system. It then elaborates on the role of the innate immune system in PD, in the context of neuroinflammation and the cellular components including microglia and astrocytes. It then explores the association between neuroinflammation, complement system, excitotoxicity, oxidative stress, dopamine metabolism, tyrosine hydroxylase and blood brain barrier in relation to PD. Finally, the review deliberates upon and proposes various diagnostic and therapeutic strategies based on the innate immune system that could be utilised to target the immunological mechanisms participating in PD.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578716"},"PeriodicalIF":2.5,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144866563","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":"Structural and functional biomarkers of visual dysfunction in MOG antibody-positive optic neuritis: a scoping review","authors":"Fiona Chan ,&nbsp;Clare Fraser ,&nbsp;Fabienne Brilot ,&nbsp;Russell C. Dale ,&nbsp;Sudarshini Ramanathan","doi":"10.1016/j.jneuroim.2025.578715","DOIUrl":"10.1016/j.jneuroim.2025.578715","url":null,"abstract":"<div><h3>Introduction</h3><div>Myelin-oligodendrocyte glycoprotein antibody-associated disease (MOGAD) commonly manifests as optic neuritis (ON) in association with serum MOG immunoglobulin G (MOG-IgG). This review will evaluate the literature on visual dysfunction in MOG-IgG ON, with a focus on ophthalmic structural biomarkers and ancillary outcome measures.</div></div><div><h3>Methods</h3><div>PubMed was systematically searched using the terms “optic neuritis”, “visual outcomes” and “myelin-oligodendrocyte glycoprotein” between 2007 to January 2025. High-contrast visual acuity (HCVA), low-contrast visual acuity (LCVA), contrast sensitivity, visual fields (VF), electrophysiology, optical coherence tomography (OCT)/angiography, magnetic resonance imaging (MRI) and quality of life (QoL) were evaluated.</div></div><div><h3>Results</h3><div>35 studies and 2335 patients were included. 89 % of studies reported HCVA. OCT and MRI were reported in 63 % and 43 % of studies, respectively. MOG-IgG ON had moderate-severe HCVA loss at nadir but good HCVA recovery. MRI features characteristic to MOG-IgG ON include longitudinally extensive lesions +/− perineural enhancement. OCT in acute MOG-IgG ON revealed moderate-severe peripapillary retinal nerve fibre layer (p-RNFL) swelling. However severe axonal loss was noted in chronic outcomes, despite preservation of HCVA, highlighting a recognised structure-function discordance. Only 31 % reported on VFs, 17 % on LCVA, and 14 % on VEPs, all of which demonstrated abnormalities even in patients with normal HCVA. Only one study reported on contrast sensitivity or QoL.</div></div><div><h3>Conclusion</h3><div>Current clinical assessments may underestimate visual dysfunction in MOG-IgG ON. Prospective, longitudinal multimodal evaluation should be a key focus for future research, to identify the most sensitive biomarkers to be incorporated into routine clinical practice. This will better identify patients at risk of adverse visual outcomes in MOG-IgG ON, guide clinical management and improve QoL.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"408 ","pages":"Article 578715"},"PeriodicalIF":2.5,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144866564","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":"Harnessing the innate immune system for glioblastoma therapeutics","authors":"Hamish McLean ,&nbsp;Matthew Drill ,&nbsp;Richard Sequeira ,&nbsp;Padmakrishnan Chorakode Jayakrishnan ,&nbsp;Rosalind L. Jeffree ,&nbsp;Martin Hunn ,&nbsp;Terence J. O'Brien ,&nbsp;John Hamilton ,&nbsp;Mastura Monif","doi":"10.1016/j.jneuroim.2025.578713","DOIUrl":"10.1016/j.jneuroim.2025.578713","url":null,"abstract":"<div><div>Glioblastoma is the most common primary malignant brain cancer and is associated with significant mortality and resistance to treatment. One of the major barriers to successful treatment of this cancer is the highly immunosuppressive tumour microenvironment. This tumour microenvironment is comprised of a complex mixture of cancerous cells, neurons, astrocytes, and a variety of immune cells. Microglia, macrophages and monocytes make up a significant proportion of the cells present in the glioblastoma tumour microenvironment. These innate immune cells normally act to maintain homeostasis, though following exposure to cancer cells are signalled to support glioblastoma cancer cell proliferation and treatment resistance. This review provides detailed insights into the role of innate immunity on glioblastoma cell proliferation and glioblastoma pathogenesis. It discusses ways of harnessing the anti-tumour potential of innate immune cells and documents the current preclinical and clinical trials focusing on innate immunity in glioblastoma. The work presented showcases how the anti-tumour capacity of innate immune cells could be utilised to provide novel treatment strategies to combat glioblastoma.</div></div>","PeriodicalId":16671,"journal":{"name":"Journal of neuroimmunology","volume":"407 ","pages":"Article 578713"},"PeriodicalIF":2.5,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826318","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}