NeuroimmunomodulationPub Date : 2026-01-01Epub Date: 2026-09-05DOI: 10.1159/nim/adxag003
Justus Mörstedt, Lev Lipovsky, Benjamin Graul, Olga Seifert
{"title":"Disease-Specific Associations of Physical Activity in Patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus.","authors":"Justus Mörstedt, Lev Lipovsky, Benjamin Graul, Olga Seifert","doi":"10.1159/nim/adxag003","DOIUrl":"10.1159/nim/adxag003","url":null,"abstract":"<p><strong>Introduction: </strong>Patients with inflammatory rheumatic diseases exhibit reduced physical activity (PA), contributing to increased cardiovascular risk and functional decline. While PA is recommended in both rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), variables associated with PA remain poorly understood. Therefore, this study explored shared and disease-specific associations with PA in RA and SLE.</p><p><strong>Methods: </strong>In this cross-sectional study, patients with RA (n = 200) and 94 SLE (n = 94), fulfilling ACR classification criteria, were recruited from the rheumatological outpatient clinic of the University Hospital Leipzig. Sociodemographic data were obtained from electronic records. Patient-reported outcome measures assessed comorbidities, PA, and health-related quality of life. PA was quantified using the International Physical Activity Questionnaire-Long Form. Associations were examined using multivariable logistic regression models.</p><p><strong>Results: </strong>Patients with RA showed lower physical performance (p < 0.001) but higher PA levels than SLE (p < 0.001). In RA, fibromyalgia remained the only statistically significant variable and was associated with lower PA (OR = 0.001, 95% confidence interval [CI]: < 0.001-0.289; p = 0.017). In SLE, no independent predictors were identified; fibromyalgia (OR = 0.374, p = 0.209) and depressive symptoms (OR = 0.341, p = 0.063) showed nonsignificant trends. Self-reported PA and objective walking performance were moderately associated in both groups (RA: R2 = 0.19; SLE: R2 = 0.12).</p><p><strong>Conclusion: </strong>Associations with PA differ between RA and SLE. In RA, fibromyalgia is associated with lower PA, whereas in SLE, PA reflects a multifactorial interplay of functional and psychological factors, supporting disease-specific approaches to PA promotion.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"338-448"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897486","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}
NeuroimmunomodulationPub Date : 2026-01-01Epub Date: 2026-01-08DOI: 10.1159/000550372
Sergueï O Fetissov
{"title":"Immune System Controls Gut Bacterial and Host Peptide Signals in Appetite Regulation: Towards Specific Immunotherapy of Eating Disorders.","authors":"Sergueï O Fetissov","doi":"10.1159/000550372","DOIUrl":"10.1159/000550372","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"5-6"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12858191/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145934078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NeuroimmunomodulationPub Date : 2026-01-01Epub Date: 2026-03-12DOI: 10.1159/000551426
Hiromi Yano, Ryo Fujii, Rikuho Tahara, Chihiro Watanabe, Hiroki Hamada, Takumi Kono, Takafumi Aoki, Michael J Kremenik, Eri Oyanagi
{"title":"Prebiotic Diet Enhances Suppression of Tumor Necrosis Factor-Alpha Production in Response to Lipopolysaccharide after Exhaustive Exercise.","authors":"Hiromi Yano, Ryo Fujii, Rikuho Tahara, Chihiro Watanabe, Hiroki Hamada, Takumi Kono, Takafumi Aoki, Michael J Kremenik, Eri Oyanagi","doi":"10.1159/000551426","DOIUrl":"10.1159/000551426","url":null,"abstract":"<p><strong>Introduction: </strong>Although it is well known that severe exercise induces temporary immunosuppression, it remains unclear the effect of gut microbiota on this phenomenon.</p><p><strong>Methods: </strong>In this study, to investigate the effect of gut microbiota on the lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production immediately after the exhaustive exercise, C3H/HeN male mice were (1) treated with or without antibiotic (AB), (2) transplanted cecal content from a 5% partially hydrolyzed guar-gum (PHGG) diet, which is classified as low viscous in dietary fiber, fed mice, and (3) intake PHGG diet for 6 weeks. The mice were stimulated by LPS administration immediately after loaded forced exhaustive exercise.</p><p><strong>Results: </strong>After the exhaustive exercise, plasma TNF-α concentration in AB mice prior to response from LPS was significantly higher than that in control mice (p < 0.01). On the other hand, differences in transplanted cecal contents did not affect TNF-α production by exercise prior to LPS administration. Direct intake of PHGG, however, attenuated the increase in plasma TNF-α concentration in response to LPS, compared with both non-fiber and control diet groups (p < 0.01).</p><p><strong>Conclusion: </strong>These results suggest that LPS-induced TNF-α production immediately after intense exercise is regulated depending on both the composition of the gut microbiota and the material being fermented.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"150-159"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13197150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147444363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NeuroimmunomodulationPub Date : 2026-01-01Epub Date: 2026-07-03DOI: 10.1159/000552735
Jordano Brito-Moreira, Edla Azevedo Herculano, Wilson Savino
{"title":"Extracellular Matrix-Mediated Neuroendocrine Control of the Thymus.","authors":"Jordano Brito-Moreira, Edla Azevedo Herculano, Wilson Savino","doi":"10.1159/000552735","DOIUrl":"10.1159/000552735","url":null,"abstract":"<p><strong>Background: </strong>The thymus is the primary lymphoid organ responsible for the generation of a self-tolerant and immunocompetent T-cell repertoire. Its function is not autonomous but is finely tuned by a complex neuroendocrine network, integrating signals from the central nervous system and the endocrine system to modulate thymopoiesis. While the roles of classical hormones and neurotransmitters in regulating thymic epithelial cell (TEC) function and T-cell development are increasingly recognized, the mechanistic pathways by which these signals are integrated within the thymic microenvironment still have much to be understood.</p><p><strong>Summary: </strong>A key, yet underexplored, component of the thymic microenvironment is the extracellular matrix (ECM). It is very clear today that ECM is not a passive scaffold but a dynamic structure that presents critical signals for thymocyte migration, proliferation, and selection. This review synthesizes current evidence to propose a novel paradigm: the thymic ECM acts as a key mediator of neuroendocrine control. We explore how specific ECM molecules, such as laminins, collagens, and fibronectin, expressed by TECs and other microenvironmental cells, can be modulated by neuroendocrine ligands.</p><p><strong>Key messages: </strong>Theses ECM modulations directly impact the presentation of key receptors, such as integrins, thereby influencing the critical crosstalk between a given thymic niche and developing lymphocytes. By delineating the ECM-mediated mechanisms, this review aimed to provide a more holistic understanding of how neuroendocrine factors govern thymic physiology, with implications for aging, stress-related immunosenescence, and therapeutic strategies aimed at thymic regeneration.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"304-314"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13466443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148382353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NeuroimmunomodulationPub Date : 2026-01-01Epub Date: 2026-02-13DOI: 10.1159/000551037
Larissa C Engert, Rammy Dang, Bryan Chatterton, Surya Daniel, Janet M Mullington, Monika Haack
{"title":"The Effect of Low-Dose Acetylsalicylic Acid on Cellular Immune Responses to Experimental Sleep Restriction in Healthy Humans.","authors":"Larissa C Engert, Rammy Dang, Bryan Chatterton, Surya Daniel, Janet M Mullington, Monika Haack","doi":"10.1159/000551037","DOIUrl":"10.1159/000551037","url":null,"abstract":"<p><strong>Introduction: </strong>Sleep deficiency is known to increase the risk for multiple disease conditions involving immunopathology, in which inflammation is thought to be a mechanism for disease development. Thus, one potential way to mitigate negative health consequences of deficient sleep is to target inflammation. We investigated whether low-dose acetylsalicylic acid (ASA, aspirin) administration prior to and during exposure to an experimental sleep restriction challenge affects cellular immune responses to sleep restriction.</p><p><strong>Methods: </strong>We studied 46 healthy humans (19F/27M, age range 19-63 years) in a randomized trial with 3 protocols each consisting of a 14-day at-home phase followed by an 11-day (10-night) in-laboratory stay (sleep restriction/ASA, sleep restriction/placebo, control sleep/placebo) with daily ASA (81 mg/day) or placebo intake across the entire study period (at-home and in-laboratory). During in-laboratory stays, sleep opportunity under both sleep restriction conditions was 8 h during 2 pre-challenge nights, 4 h during 5 nights of restricted sleep, and 8 h during 3 nights of recovery sleep. Under the control sleep condition, participants had a sleep opportunity of 8 h/night throughout the protocol. Blood samples were analyzed prior to and following 5 nights of sleep restriction/control sleep, and after 2 nights of recovery sleep. Data were analyzed using generalized linear mixed models.</p><p><strong>Results: </strong>Experimental sleep restriction increased WBC, lymphocyte, monocyte, eosinophil, basophil, CD4 T-cell counts, and the CD4/CD8 T-cell ratio compared to control sleep under placebo (p < 0.01). Low-dose ASA had no effect at pre-challenge for most cell types. However, low-dose ASA attenuated the eosinophil and basophil responses to sleep restriction and reduced elevation of the CD4/CD8 T-cell ratio (p < 0.01). Monocyte counts stayed elevated after 2 nights of recovery sleep in the sleep restriction/ASA condition compared to control sleep, whereas monocyte counts recovered under placebo intake (p < 0.01).</p><p><strong>Conclusion: </strong>The present study shows that low-dose ASA can counteract certain cellular immune responses to sleep restriction, in particular elevations in eosinophil and basophil counts as well as the CD4/CD8 T-cell ratio, while not affecting most immune cell counts prior to the sleep restriction challenge.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"125-137"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13014424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146195401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NeuroimmunomodulationPub Date : 2026-01-01Epub Date: 2026-09-09DOI: 10.1159/nim/adxag004
Alexander Karabatsiakis, Lisa Holper, Felix Scholkmann
{"title":"The Importance of the Individual Baseline Immunometabolic and Cerebrovascular State in Correctly Interpreting Functional Neuroimaging Data: Lessons from Blood Mitochondrial Respirometry.","authors":"Alexander Karabatsiakis, Lisa Holper, Felix Scholkmann","doi":"10.1159/nim/adxag004","DOIUrl":"10.1159/nim/adxag004","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"355-359"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920803","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}
NeuroimmunomodulationPub Date : 2026-01-01Epub Date: 2025-12-16DOI: 10.1159/000550042
Kati Wiedenbrüg, Lisa Musculus, Celine Hilpisch, Sebastian Hacker, Karsten Krüger
{"title":"Inflammation and Perceived Social Support in Elite Athletes (A Quantile Regression Approach).","authors":"Kati Wiedenbrüg, Lisa Musculus, Celine Hilpisch, Sebastian Hacker, Karsten Krüger","doi":"10.1159/000550042","DOIUrl":"10.1159/000550042","url":null,"abstract":"<p><strong>Introduction: </strong>Inflammation and social relationships are bidirectionally linked, yet evidence in young, nonclinical populations is scarce. Given that elite athletes face continuous immune challenges and unique social conditions, this cohort provides a model to explore this association.</p><p><strong>Methods: </strong>Several quantile regressions were computed across 422 elite athletes. To account for both the magnitude of inflammation and the characteristics of social relationships, quantiles were determined based on the concentrations of tumor necrosis factor alpha, interleukin-6, and the systemic inflammatory response index (SIRI) as well as on measures of the total, general perceived social support. The corresponding predictors were social support and the inflammatory markers.</p><p><strong>Results: </strong>A higher total, general perceived social support predicted a significantly lower SIRI in the lowest quartile as well as lower concentrations of the cytokines in the highest three quartiles. Effects were small but robust. Moreover, higher inflammation predicted a lower total, general perceived social support in elite athletes, when the perceived social support was relatively moderate. However, this effect was not robust when covariates, such as urea or the living situation, were added to the models.</p><p><strong>Conclusion: </strong>Results suggest that elite athletes' social relationships are a small yet important factor influencing the inflammatory response. The social support elite athletes perceive, however, appears to be influenced by inflammation only under specific biopsychosocial conditions.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"19-33"},"PeriodicalIF":2.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12880831/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145768685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
NeuroimmunomodulationPub Date : 2026-01-01Epub Date: 2026-02-09DOI: 10.1159/000549975
Stefanie Hölsken, Eva Holubek, Frederik Krefting, Senta Mühlhaus, Daniela Bese, Joachim Dissemond, Oliver Pfaar, Winfried Rief, Manfred Schedlowski, Wiebke Sondermann
{"title":"Experimental Approach to Inducing Anti-Histaminergic Placebo Effects: A Randomized Controlled Trial in Healthy Volunteers.","authors":"Stefanie Hölsken, Eva Holubek, Frederik Krefting, Senta Mühlhaus, Daniela Bese, Joachim Dissemond, Oliver Pfaar, Winfried Rief, Manfred Schedlowski, Wiebke Sondermann","doi":"10.1159/000549975","DOIUrl":"10.1159/000549975","url":null,"abstract":"<p><strong>Introduction: </strong>Allergies are an increasingly widespread health problem and prior evidence suggests that psychological factors are involved in their occurrence and alleviation. This study aimed to investigate how placebo treatment can reduce type-I allergic symptoms in a skin prick test in healthy volunteers.</p><p><strong>Methods: </strong>Healthy volunteers of all genders were included in the study (N = 88) and were randomized into three groups: (i) a classically conditioned group receiving the anti-histaminergic drug cetirizine as unconditioned stimulus (US) and a novel gustatory stimulus as conditioned stimulus (CS), (ii) a context-control group receiving cetirizine (US) and water as CS and (iii) an open-label placebo group. In the spirit of the ethical application of placebo, participants were not blinded with regard to the study question. Histamine skin prick tests were conducted at baseline, after five acquisition trials, before evocation, as well as after three and five evocation trials. Self-rated itch and wheal size measurements served as outcome parameters.</p><p><strong>Results: </strong>Itch was significantly reduced after medication and (open) placebo intake. Wheal size was only reduced significantly after medication intake during acquisition. After 9 days of washout, itch ratings were lower in participants who had received open-label placebo compared to those who had initially received cetirizine. During the evocation week, the decline in wheal size did not reach statistical significance and there was no significant differential effect of group allocation. Reported expectations of symptom relief at the last visit correlated positively with reductions of wheal size, but results were substantially influenced by outliers. Expectations of relief could partially be explained by participants' prior experiences and group allocation.</p><p><strong>Conclusion: </strong>Participants of all groups experienced a reduction in itch, while wheal size was only reduced in those participants with high expectations. These expectation effects align with prior research but should be carefully tested in future studies. Taken together, these results support the theory of differing mechanisms between patients with lived experience and healthy participants. Future studies should investigate the underlying neuropsychological mechanisms of expectation-induced anti-histaminergic effects.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"75-88"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13002230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146150163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Taselisib, a PI3K Inhibitor, Alleviates Neuropathic Pain through HIF-1α-Mediated Angiogenesis in a Rat Model of Chronic Constriction Injury.","authors":"Hai-Ping You, Li-Hong Zhang, Chui-Yu Li, He-Fan He, Zhi-Yuan Chen, Hong-Geng Wang, Wei-Feng Liu, Chong-Jun Xu","doi":"10.1159/nim/adxag005","DOIUrl":"10.1159/nim/adxag005","url":null,"abstract":"<p><strong>Introduction: </strong>Neuropathic pain is associated with hypoxia, inflammation, and metabolic dysregulation, in which hypoxia-inducible factor-1α (HIF-1α) plays a key regulatory role. This study investigates whether phosphoinositide 3-kinase (PI3K) inhibition by taselisib alleviates neuropathic pain via suppression of HIF-1α-mediated pathological signaling.</p><p><strong>Methods: </strong>In this study, a rat model of chronic constriction injury (CCI) was used to investigate whether neuropathic pain could be alleviated by taselisib, a selective PI3K inhibitor. Taselisib was administered daily, with or without co-administration of dimethyloxalylglycine (DMOG), a HIF-1α activator. Mechanical allodynia and thermal hyperalgesia were evaluated using behavioral tests. mRNA level in the dorsal root ganglia (DRG) was quantified by RT-qPCR, whereas protein levels were assessed by Western blotting, immunofluorescence, and metabolic assays were performed to assess angiogenesis, glycolytic activity, and inflammatory responses.</p><p><strong>Results: </strong>Taselisib significantly alleviated mechanical allodynia and thermal hyperalgesia in CCI rats, effects that were attenuated by co-administration of the HIF-1α activator DMOG. Taselisib suppressed CCI-induced upregulation of HIF-1α in DRG at both transcript and protein levels, and this suppression was reversed by DMOG. Downstream targets of HIF-1α, including mTOR, VEGFA, GLUT1, PFKM, and PDK1, were similarly downregulated by taselisib and partially restored upon HIF-1α activation. Metabolically, taselisib reduced lactate accumulation and restored ATP levels, indicating inhibition of glycolytic reprogramming. Taselisib also attenuated systemic and DRG-localized inflammatory responses, including IL-6, IL-1β, and NF-κB p65 expression; these anti-inflammatory effects were mitigated by DMOG.</p><p><strong>Conclusion: </strong>Taselisib alleviates neuropathic pain by disrupting HIF-1α-mediated angiogenic, inflammatory, and metabolic signaling. Targeting the PI3K-HIF-1α axis offers a promising therapeutic approach.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"360-371"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920745","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}
NeuroimmunomodulationPub Date : 2025-01-01Epub Date: 2025-04-02DOI: 10.1159/000545633
Maurizio Cutolo, Stefano Bombardieri, Rainer H Straub, Johannes W J Bijlsma, Frank Buttgereit
{"title":"In Memoriam: Alfonse T. Masi, MD.","authors":"Maurizio Cutolo, Stefano Bombardieri, Rainer H Straub, Johannes W J Bijlsma, Frank Buttgereit","doi":"10.1159/000545633","DOIUrl":"10.1159/000545633","url":null,"abstract":"","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":" ","pages":"124-125"},"PeriodicalIF":2.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772922","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}