BackgroundThis study investigates the pathogenic contributions of aquaporin-4 (AQP4)-specific follicular helper T (Tfh) and T helper 17 (Th17) cells in neuromyelitis optica spectrum disorder (NMOSD), utilizing newly established murine models based on adoptive transfer of antigen-specific T-cell populations.MethodsAQP4-knockout mice were immunized with the AQP4-derived peptide to generate AQP4-reactive Tfh and Th17 cells. These cells were subsequently isolated and adoptively transferred into wild-type recipient mice. At disease peak—defined by consistent neurological deficits—spinal cord and brain tissues were harvested for histopathological analysis, as well as immunohistochemistry. Central nervous system immune cell infiltration was quantified via flow cytometry. Total RNA was extracted from spinal cord tissue for bulk RNA sequencing; differentially expressed genes were validated using quantitative real-time PCR.ResultsRecipient mice that received AQP4-reactive Tfh or Th17 cells developed progressive hind-limb weakness, with Th17-transferred mice exhibiting significantly more severe clinical scores. Histopathological analyses revealed robust perivascular inflammation, parenchymal immune infiltration, and focal demyelination. Immunohistochemical quantification demonstrated significantly increased the optical density of CD3, B220, GFAP, IBA1, and CXCL9, alongside markedly decreased MBP expression. Flow cytometric profiling confirmed substantial infiltration of leukocytes and activated microglia/macrophages into the central nervous system (CNS). Transcriptomic analysis identified CXCL9 as one of the most upregulated chemokines in the spinal cord; its astrocytic origin was further corroborated by confocal immunofluorescence co-localization with GFAP.ConclusionOur findings establish that AQP4-specific Tfh and Th17 cells are sufficient to drive key neuropathological features of NMOSD—including microglial reactivity, leukocyte recruitment, neuroinflammation, and demyelination—in vivo. The pronounced upregulation and astrocyte-derived expression of CXCL9 suggest its involvement in orchestrating CNS inflammation and position it as a potential contributor for NMOSD.

Background:This study aimed to compare the proportions of circulating follicular helper T (Tfh) and B cell subsets, as well as serum levels of cytokines and chemokines, between patients with neuromyelitis optica spectrum disorder (NMOSD) who are anti-aquaporin-4 antibody (AQP4-ab)-positive and healthy controls, and to investigate the interaction mechanisms between Tfh and B cells. Methods:AQP4-ab-positive NMOSD patients were enrolled during acute attacks and remission phases, along with age- and sex-matched healthy controls. Flow cytometry was used to assess circulating Tfh and B cell subsets. Purified CD19+ B cells were cultured alone or co-cultured with CD4+CXCR5+ Tfh cells for 6 days, with various interventions applied to evaluate alterations in Tfh or B cell phenotypes. Serum and supernatant levels of interleukin (IL)-6, IL-21, CXCL13, and AQP4-ab were measured. Results:During acute attacks, NMOSD patients exhibited significantly higher proportions of total Tfh, ICOS+ Tfh, activated Tfh17, switched memory B cells, double-negative B cells, plasmablasts, and plasma cells, along with elevated serum levels of IL-6, IL-21, and CXCL13. In contrast, the frequencies of activated Tfh1, naive B cells, and transitional regulatory B cell subsets were significantly reduced. Functional assays revealed that Tfh cells promoted B cell proliferation, differentiation, and AQP4-ab production. Conversely, B cell subsets enhanced Tfh cell proliferation, differentiation, and IL-21 secretion; these effects were attenuated by anti-CD20 and anti-interferon-γ (IFN-γ) monoclonal antibodies, but were augmented by anti-IL-10 monoclonal antibody. Conclusions:Circulating Tfh and B cell subsets are dysregulated in AQP4-ab-positive NMOSD, accompanied by increased levels of IL-6, IL-21, and CXCL13. Reciprocal interactions between Tfh and B cells likely contribute to disease pathogenesis.

Background:Inebilizumab was included in China's national reimbursement drug list in 2023, enhancing its accessibility. However, there is a paucity of real-world data evaluating its performance in Chinese patients with aquaporin-4 immunoglobulin G-seropositive neuromyelitis optica spectrum disorder (AQP4-IgG+ NMOSD). This prospective study therefore sought to assess the treatment outcomes and identify predictive factors for relapse and severe pneumonia in Chinese patients treated with Inebilizumab. Methods:This study enrolled AQP4-IgG+ NMOSD patients receiving ≥1 dose of inebilizumab from March 2023 to June 2025. The primary outcome was time to first relapse. Secondary outcomes included annualized relapse rate (ARR), Expanded Disability Status Scale (EDSS) score, drug retention rates, and adverse events (AEs). Multivariate regression analyses were conducted to identify predictors of relapse and severe pneumonia. Results:Among 136 patients (91.9% female; mean age 40.3 years; median treatment duration 13.8 months), the 12-month relapse-free rate was 88.1% (95% confidence interval [CI] =82.1-94.5%). Thirteen patients experienced 14 relapses, with 7 occurring within the first 6 months. The median time to first relapse was 5.2 months (range, 0.3-11.8). Risk factors for relapse within 12 months included: age at onset ≤ 20 years (hazard ratio [HR] 8.17, 95% CI = 1.96-34.03, p=0.004), disease duration >5 years (HR 8.06, 95% CI = 1.72-37.83, p=0.008), and pre-treatment relapses (HR 3.04, 95% CI = 1.32-6.98, p=0.009). The annualized relapse rate (ARR) significantly decreased (1.496 vs 0.117, p<0.001). The median EDSS score decreased (from 2.5 to 2.0, p = 0.002) in patients who started inebilizumab during the remission phase. The 12-month drug retention rate was 88.9% (95% CI 82.8-95.5%). Seven patients developed severe pneumonia, significantly associated with baseline EDSS ≥6.5 (odds ratio [OR] 25.4, 95% CI = 2.12-334, p=0.013) and IgG <6 g/L (OR 14.2, 95% CI = 1.79-136, p=0.007). Conclusion:This study confirms the real-world effectiveness of inebilizumab in Chinese NMOSD patients but identifies distinct clinical profiles for relapse and infection risk. Patients with early-onset, long-standing, or highly active disease are at greater risk of breakthrough relapses, whereas those with high disability and hypogammaglobulinemia require vigilance for severe pneumonia. These findings advocate for a risk-stratified management approach to optimize treatment outcomes.

Efgartigimod is a neonatal Fc receptor (FcRn) inhibitor that primarily diminishes antibody levels by inhibiting antibody (IgG) reabsorption and is noted for its rapid onset of action and low immunogenicity. Currently, efgartigimod is approved for the treatment of anti-acetylcholine receptor (AChR) antibody-positive generalized myasthenia gravis (gMG), yet there are no relevant clinical trials for myasthenic crisis (MC). Consequently, we performed a systematic review of the available literature to evaluate the clinical efficacy of efgartigimod for the treatment of MC. We conducted a search of the PubMed, Web of science, Embase, and Scopus databases for all observational studies published until September 30, 2024. Risk of bias was assessed using the Joanna Briggs Institute (JBI) Case Report and Series Critical Assessment Checklist for quality assessment of included studies. A total of nine case reports/series, all observational studies, were included. Twenty MC patients were included, all of whom exhibited clinically significant improvement after treatment with Efgartigimod, with a sustained decrease in AChR antibody serum titers and a significant decrease in IgG levels throughout the treatment cycle. Efgartigimod demonstrates favorable clinical efficacy. Efgartigimod may serve as an effective treatment for patients with MC. However, further studies are required to clarify the efficacy of Efgartigimod alone. PROSPERO registration number: CRD42023430032

To evaluate the relationship between aquaporin-4 immunoglobulin G (AQP4-IgG) titer dynamics and relapse in neuromyelitis optica spectrum disorder (NMOSD), compare AQP4-IgG dynamics across different maintenance therapy strategies, and identify factors associated with AQP4-IgG titer seroreversion to negativity. Altogether 171 patients with ≥ 2 serum AQP4-IgG tests by fixed cell-based assay 30 days apart and at least once positive were included. Their clinical and treatment data were reviewed. Among the 171 NMOSD patients with a median disease duration of 81.3 months, 44 (25.7

Objective:To assess clinical outcomes in patients treated with eculizumab for acute attacks of aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (NMOSD). Methods:We retrospectively analyzed prospectively collected data from the Huashan NMOSD registry cohort, and included patients who received eculizumab within 30 days of attack onset. Eculizumab was administered at 900 mg weekly for four weeks, followed by an eight-week observation period. Primary outcomes included visual acuity and visual field for optic neuritis (ON) and muscle strength, assessed using the Medical Research Council (MRC) scale for longitudinally extensive transverse myelitis (LETM). Serum neurofilament light chain (sNfL) and glial fibrillary acidic protein (sGFAP) levels were also monitored. Results:Nine patients (seven with ON, two with LETM) were included. All patients received high-dose intravenous methylprednisolone prior to eculizumab treatment. Following eculizumab, six of the seven ON patients showed significant improvements in visual acuity and visual fields, with five recovering to near-normal or pre-attack vision. Visual field mean deviation improved from -22.4 dB to -2.0 dB (p = 0.008). Among LETM patients, one regained substantial lower limb strength (MRC grade 0 to 3 proximally, 4 distally), while the other showed improvement in distal strength (MRC grade 0 to 3). Serum sGFAP decreased from 278.0 to 130 pg/mL (p = 0.027), while sNfL levels transiently increased before stabilizing. One LETM patient developed a urinary tract infection, and another had Klebsiella pneumoniae pneumonia; all infections were effectively treated. Conclusion:Eculizumab may yield favorable outcomes in acute NMOSD attacks, with infection monitoring being particularly important in severe cases.

BACKGROUND:To delineate the clinical characteristics and outcomes of late-onset myelin oligodendrocyte glycoprotein antibody-associated disease (LO-MOGAD) and compare them with those of early-onset MOGAD (EO-MOGAD). METHODS:This observational cohort study included 199 adult patients with MOGAD. We reviewed the patients' demographic and clinical data and performed comparative analyses between EO-MOGAD and LO-MOGAD (onset age 18-50 and ≥50 years, respectively). RESULTS:Among the 199 patients, 42 had LO-MOGAD. Compared with patients with EO-MOGAD, those with LO-MOGAD patients exhibited a significantly higher incidence of optic neuritis both at the initial attack (66.67% vs 43.31%, p=0.007) and throughout all attacks (72.15% vs 52.51%, p=0.001). Over a similar disease duration, patients with LO-MOGAD exhibited significantly fewer relapsing courses (45.16% vs 70.97%), higher Expanded Disability Status Scale (EDSS) and visual functional system scores at the last visit (all p<0.05). Compared with patients with EO-MOGAD, those with LO-MOGAD had a significantly lower risk of relapse (HR 0.512, 95% CI 0.268 to 0.978, p=0.034), but higher risks of reaching EDSS ≥2 (HR 2.893, 95% CI 1.524 to 5.494, p<0.001) and visual acuity ≤0.6 (HR 3.097, 95% CI 1.073 to 8.937, p=0.022). Immunosuppressive therapies significantly reduced the annualised relapse rates of patients with LO-MOGAD, although adverse events leading to drug discontinuation and hospitalisation were observed. CONCLUSIONS:Compared with patients with EO-MOGAD, patients with LO-MOGAD exhibited fewer relapsing courses but worse disability outcomes and should be actively treated.

BACKGROUND AND PURPOSE:Prodromal infections are associated with neuromyelitis optica spectrum disorder (NMOSD), but it remains unclear which type of infection has a causal association with NMOSD. We aimed to explore the causal associations between four herpesvirus infections (chickenpox, cold sores, mononucleosis and shingles) and NMOSD, as well as between other types of infections and NMOSD.METHODS:For data on infections, we used the genome-wide association study (GWAS) summary statistics from the 23andMe cohort. For outcomes, we used the GWAS data of participants of European ancestry, including 215 NMOSD patients (132 anti-aquaporin-4 antibody [AQP4-ab]-positive patients and 83 AQP4-ab-negative patients) and 1244 normal controls. Single-nucleotide polymorphism (SNP) identification and two-sample Mendelian randomization (MR) analyses were then performed.RESULTS:In the 23andMe cohort, we identified one SNP for chickenpox (rs9266089 in HLA-B gene), one SNP for cold scores (rs885950 in the POU5F1 gene), one SNP for mononucleosis (rs2596465 in the HCP5 gene), and three SNPs for shingles (rs2523591 in the HLA-B gene; rs7047299 in the IFNA21 gene; rs9260809 in the MICD gene). The association between cold sores and AQP4-ab-positive NMOSD reached statistical significance (odds ratio [OR] 745.318; 95% confidence interval [CI] 22.176, 25,049.53 [p < 0.001, Q < 0.001]). The association between shingles and AQP4-ab-positive NMOSD was also statistically significant (OR 21.073; 95% CI 4.271, 103.974 [p < 0.001, Q < 0.001]). No significant association was observed between other infections and AQP4-ab-positive or AQP4-ab-negative NMOSD.CONCLUSION:These findings suggest there are positive associations between cold sores and shingles and AQP4-ab-positive NMOSD, indicating there may be causal links between herpes simplex virus and varicella-zoster virus infection and AQP4-ab-positive NMOSD.

Objectives:To examine the short-term and mid-term effects of surgical treatment of obstructive hypertrophic cardiomyopathy (HCM) in one center.Methods:The perioperative data and short-term follow-up outcomes of 421 patients with obstructive HCM who received surgical treatment at Department of Cardiac Surgery, Zhongshan Hospital, Fudan University from January 2017 to December 2021 were analyzed retrospectively. There were 207 males and 214 females, aged (56.5±11.7) years (range: 19 to 78 years). Preoperative New York Heart Association (NYHA) classification included 45 cases of class Ⅱ, 328 cases in class Ⅲ, and 48 cases in class Ⅳ. Fifty-eight patients were diagnosed with latent obstructive HCM and 257 patients had moderate or more mitral regurgitation with 56 patients suffering from intrinsic mitral valve diseases. All procedures were completed by a multidisciplinary team, including professional echocardiologists involving in preoperative planning for proper miitral valve management strategies and intraoperative monitoring. A total of 338 patients underwent septal myectomy alone, and 59 patients underwent mitral valve surgery along with myectomy. A single transaortic approach was used in 355 patients, and a right atrial-atrial septal/atrial sulcus approach was used in 51 other patients. Long-handled minimally invasive surgical instruments were wsed for the procedures. Student t test, Wilcoxon rank sum test, χ2 test or Fisher exact test were used to compare the data before and after surgery. Results:The aortic cross-clamping time of septal myectomy alone was (34.3±8.5) minutes (range: 21 to 94 minutes). Eighteen patients had intraoperative adverse events and underwent immediate reoperation, including residual obstruction (10 patients), left ventricular free wall rupture (4 patients), ventricular septal perforation (3 patients), and aortic valve perforation (1 patient). Four patients died during hospitalization, and 11 patients developed complete atrioventricular block requiring permanent pacemaker implantation. After discharge, 384 (92.1%) patients received a follow-up visit with a median duration of 9 months. All follow-up patients survived with significantly improved NYHA classifications: 216 patients in class Ⅰ and 168 patients in class Ⅱ ( χ2=662.73, P<0.01 as compared to baseline). At 6 months after surgery, follow-up echocardiography showed that the thickness of the ventricular septum ((13.6±2.5) mm vs. (18.2±3.0) mm, t=23.51, P<0.01) and the peak left ventricular outflow tract gradient ((12.0±6.3) mmHg vs. (93.4±19.8) mmHg, 1 mmHg=0.133 kPa, t=78.29, P<0.01) were both significantly lower than baseline values. Conclusion:The construction of the surgical team (including echocardiography experts), proper mitral valve management strategies, identification and management of sub-mitral-valve abnormalities, and application of long-handled minimally invasive surgical instruments are important for the successful implementation of septal myectomy with satisfactory short-and medium-term outcomes.

Objective To characterize Takayasu arteritis (TA) with supra-aortic involvement and determine the associations between clinical features, carotid ultrasonographic (US) variables, and neurological severe ischemic events (SIEs). Methods Patients with supra-aortic involvement including brachiocephalic trunk, bilateral common carotid artery and internal carotid artery, and bilateral subclavian and vertebral artery and baseline carotid US examination were enrolled from the East China TA cohort. Bilateral carotid diameter, intima-media thickness (IMT), and peak systolic velocity (PSV) were measured by US. Then, the IMT/diameter ratio (IDR) was calculated. Risk factors associated with neurological SIEs were analyzed by multivariate logistic regression. Results In total, 295 patients were included, of whom 260 (88.14%) were female, and 93 (31.53%) experienced neurological SIEs. Involved supra-aortic artery distribution ( P = 0.04) and number ( P < 0.01) differed between subjects with neurologic and nonneurologic SIEs, showing higher prevalence of common carotid and vertebral artery involvement after Bonferroni correction and 56.99% patients having ≥ 4 involved arteries in the neurological SIE group. The bilateral IDR ( P < 0.01) differed between patients with and without neurological SIEs. The carotid IDR (left: cut-off value ≥ 0.55, OR 2.75, 95% CI 1.24–6.07, P = 0.01; right: ≥ 0.58, OR 2.70, 95% CI 1.21–6.02, P = 0.01) and left carotid PSV (≤ 76.00 cm/s, OR 3.09, 95% CI 1.53–6.27, P < 0.01), as well as involved supra-aortic artery number (≥ 4, OR 2.33, 95% CI 1.15–4.72, P = 0.02) were independently associated with neurological SIEs. Conclusion The carotid IDR and PSV might be performed as valuable markers for recognizing neurological SIEs in patients with TA with supra-aortic lesions.

Background: DLBCL (diffuse large B cell lymphoma) is the most common subtype of non-Hodgkin lymphoma (NHL). After anthracycline-based chemotherapy, more than 70% of DLBCL patients can get complete response or partial response, but only 50% - 60% of patients can survive for a long time. Adaptor Related Protein Complex 2 Subunit Mu 1 (AP2M1) encodes a subunit of the hetero tetrameric coat assembly protein complex 2 (AP2), which required for the activity of a vacuolar ATPase and may also play an important role in regulating the intracellular trafficking and function of CTLA-4 protein. There are few reports on the relationship between DLBCL and AP2M1. Meanwhile, it is unclear whether it is related to the pathogenesis of DLBCL. Aims: Here, in this study, the relationship between DLBCL and AP2M1 and its effect in DLBCL chemotherapy were studied. Methods: Using public datasets of DLBCL from both GEO and TCGA databases, we analyzed the role of AP2M1 in mediating chemoresistance to R-CHOP and its correlation with various clinical parameters and prognosis. By using various R packages, we evaluated the role of AP2M1 on regulating tumor immune microenvironment. Moreover, FFPE samples of DLBCL from Beijing Tongren Hospital were used to valiate our findings. Results: We found that the expression of AP2M1 was significantly increased in DLBCL, which was correlated with poor prognosis and a variety of clinical indicators. On the basis of enrichment analysis, it was found that AP2M1 may be related to intracellular receptor signaling pathway. Through immune analysis and drug prediction, we found that the expression of AP2M1 affected the immune environment and drug response of DLBCL, which further revealed the important role of AP2M1 in DLBCL. Using FFPE DLBCL samples from patients treated in our center, we validated the above findings that high expression of AP2M1 correlated with inferior survival outcomes and affected sensitivity to R-CHOP treatment. Image:Summary/Conclusion: In this study, we found that the expression of AP2M1 could affect the prognosis of DLBCL patients by affecting the immune environment, and the expression of AP2M1 affected the response of many drugs in DLBCL treatment, indicating AP2M1 as a potential therapy target in DLBCL.

视神经脊髓炎谱系病(NMOSD)是严重的致残性中枢神经系统自身免疫性疾病.多为复发型病程,残疾进展呈发作依赖性,预防复发NMOSD的维持治疗是缓解期治疗的关键.2019年起NMOSD维持治疗取得突破性进展,3种靶向药物相继获批适应证.当前维持治疗种类繁多,传统的超适应证和新型药物的适应证并存,尚缺乏对相关研究的总结.文中从传统非特异性免疫抑制剂及特异性靶向药物角度对NMOSD维持治疗药物的疗效性及安全性作综述.

Objective This study aimed to analyze biomarker changes in patients with TAK following treatment with glucocorticoids (GCs) and tofacitinib (TOF). Methods Seventeen patients from a prospective TAK cohort treated with GCs and TOF and 12 healthy individuals were recruited. TAK associated cytokines, chemokines, growth factors, and MMPs were analyzed in these patients before and after GCs and TOF treatment, and healthy controls. Molecular signatures associated with clinical features were evaluated. Results Patients’ cytokines (PTX3, IL-6, IFN-γ), chemokines (IL-16, CCL22, CCL2), growth factors (VEGF), and MMP9 levels were significantly higher at baseline (all p < 0.05), while patients’ FGF-2 levels were significantly lower (p = 0.02). After treatment, IL-10 was significantly increased at 6 months (p=0.007), and inflammatory cytokines such as PTX3, IL-6 demonstrated a downward trend. Patients without vascular occlusion had higher baseline CCL22 levels than patients with it (p = 0.05), which remained persistently higher after treatment. Radar plot analysis demonstrated that PTX3 was closely correlated with disease activity. In addition, patients without imaging improvement had relatively higher baseline levels of CCL22, FGF-2, and PDGF-AB (p = 0.056, p = 0.06 and p = 0.08 respectively) and lower baseline levels of TNFα, ESR, and CRP (p=0.04, p=0.056, p=0.07, respectively) compared with patients without it. Conclusion GCs and TOF are effective in decreasing inflammatory molecules but have limited efficacy in regulating multiple other markers involved in TAK. PTX3 is a prominent marker for disease activity, and CCL22 may have a predictive value for vascular progression.

OBJECTIVE:To describe the clinical features of neuromyelitis optica spectrum disorder (NMOSD) through patient registry in Yangtze River Delta area of China. METHODS:A total of 502 consecutive patients diagnosed with aquaporin-4 antibody (AQP4-ab)-positive NMOSD were registered between December 2018 to January 2021 in multiple tertiary referral centers within the framework of Yangtze River Delta of China. Their baseline data were reviewed, and follow-up clinical information were collected prospectively. RESULTS:The mean age at onset was 37.3 (range 3-80 years) years and the female-to-male ratio was 8.1:1. The median disease duration was 47 months (interquartile range [IQR] 25-84 months). A total of 1372 attacks of the 502 patients were recorded till the last follow-up, with a median annualized relapse rate of 0.4 (IQR 0.3-0.6). Nearly one-fourth (24.5%, 336/1372) of the attacks had prodromic events, including upper respiratory tract infection (36.3%, 122/336), fever (20.2%, 68/336) and pregnancy-related issues (17.9%, 60/336), etc. Myelitis was the most common attack type throughout the disease course (51.4%, 705/1372), followed by optic neuritis (ON, 43.1%, 592/1372). As for onset phenotype, ON (37.3%, 187/502) prevailed over myelitis (28.3%, 142/502). The median time to first relapse was 12 months (IQR 5-25 months). Patients with brainstem encephalitis at onset were more likely to have other anatomical region involved in subsequent attacks (p < 0.001), compared to other onset type. The median serum AQP4-ab titer measured by cell-based assays was 1:100 (IQR 1:32-1:320, range 1:10-1:10,000). The baseline AQP4-ab titer in cerebrospinal fluid (r = 0.542, p <0.001), overall ARR (r = 0.232, p< 0.001) and the EDSS scores at last follow-up (r = 0.119, p = 0.022) significantly correlated with baseline serum AQP4-ab titer. Antinuclear antibodies (48.4%), thyroid peroxidase antibodies (30.7%), and anti-SSA antibodies (26.2%) represented the most frequent concomitant antibodies, while autoimmune thyroid disorders (13.1%, 66/502) and Sjogren's syndrome (10.8%, 54/502) were the most common accompanying autoimmune diseases. Till the last follow-up, 403 patients received preventive treatments. Azathioprine represented the most common initial treatment, mycophenolate mofetil and rituximab was the most common second and third-line treatment, respectively. The EDSS score at the last follow-up ranged from 0 to 8.5 with a median of 2 (IQR 1-3). CONCLUSIONS:A comprehensive clinical picture of patients with AQP4-ab-positive NMOSD in Yangtze River Delta area of China was presented. More information on disease tragedy and predictive prognostic factors could be generated through long-term observations.

多发性硬化（MS）的疾病管理是一个长期过程，动态监测疾病活动和评估治疗反应，制定个体化MS全程管理方案成为临床所需。在传统检测方法基础上，分子生物标志物的探索和发展能更好地为MS个性化的早期疾病预、诊断、预后预测、动态评估疾病活动状态和治疗反应/安全性提供依据。MS生物标志物的检测样本主要来源于脑脊液和血液，虽然脑脊液检测特异性更高且应用更为成熟，但血液检测较脑脊液检测更为安全便捷，因此更适合用于MS疾病过程中的动态监测。同时，单分子阵列免疫分析等新型检测技术的应用能检测出血液中极低浓度的关键MS生物标志物，为研究血液生物标志物奠定了基础。文中聚焦分析血液动态检测的优势，对现有的MS血液生物标志物研究证据进行综述，探讨血液生物标志物检测在MS长期疾病管理中的临床应用价值，以期为临床实践和未来的研究提供参考。