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Therapeutic Apheresis

Oral Abstract Session - Therapeutic and Donor Apheresis and Blood Donation Infectious Disease

#OA1-AM25-TU-20 - Evaluation of Lymphoplasmapheresis as a Novel Therapy for Efficacy and Immunomodulatory Mechanisms in Neuromyelitis Optica Spectrum Disorder

Tuesday, October 28, 2025

9:30 AM - 11:00 AM PT

Room: SDCC 28BCDE

Presenting Author(s)

Siya Pei, 0009-0007-9628-7024 (she/her/hers)

Department of Blood Transfusion, Xiangya Hospital, NHC Key Laboratory of Cancer Proteomics, Central South University, Changsha, Hunan Province, China
changsha, Hunan

Disclosure information not submitted.

Background/Case Studies: Neuromyelitis optica spectrum disorders (NMOSD) are severe autoimmune central nervous system (CNS) diseases characterized by astrocyte damage, AQP4-IgG autoantibody involvement, and inflammatory cascades. Lymphoplasmapheresis (LPE), a blood purification technique removing abnormal lymphocytes and pathogenic factors, has shown promise in improving neurological function in NMOSD. This study systematically evaluates LPE’s efficacy and immune mechanisms in NMOSD through clinical, animal, and cellular experiments, integrating multi-omics and imaging techniques.

Study

Design/Methods: To investigate LPE's efficacy and immunomodulatory mechanisms in NMOSD. First, NMOSD rat models were induced with myelin basic protein and AQP4-IgG, and LPE's effects were assessed via neurological scoring (NSS), spinal cord histology (HE/LFB staining), immunofluorescence, and PET-CT/MRI. Second, a cohort of 39 AQP4-IgG-positive NMOSD patients (11 receiving standard pharmacotherapy (NMOSD-PT) and 28 treated combined PT with LPE (NMOSD-LPE)) was enrolled to compare clinical outcomes, including Expanded Disability Status Scale (EDSS) scores and cytokine profiles. Finally, immunomodulatory mechanism analysis included Mendelian Randomization (MR) was applied to explore the causal associations between 731 immune cell subtypes, 46 inflammatory mediators, and NMOSD; Mass Cytometry (CyTOF) and Flow Cytometry (FC) were used to analyze and verified T/B cell subset dynamics changes pre/post-LPE.

Results/Findings:

LPE treatment significantly improved NSS scores, reduced spinal inflammation/demyelination, restored AQP4 expression, alleviated astrocyte activation, and normalized brain metabolism/inflammation via PET-CT/MRI compared with NMOSD model rats. Clinically, NMOSD-LPE showed 0.78 decrease in EDSS scores compared with NMOSD-PT, after adjusting for confounders using multiple linear regression (p < 0.05), and lymphocyte counts post-LPE (p < 0.05). MR linked NMOSD to 43 immune cells and 2 inflammatory mediators (p < 0.05). The analysis of CyTOF and FC data from NMOSD-LPE demonstrated revealed increased levels of central memory CD4⁺ T cells (CD4⁺Tcm) and Tregs, alongside a significant reduced in 17 inflammatory mediators (p < 0.05). Furthermore, by integrating MR, CyTOF and FC data, consistent changes across methodologies highlight showed that LPE treatment increased protective CD4⁺Tcm and Treg, reduced levels of IL-6 and CCL21(CCR7 ligand).

Conclusions:

LPE improves NMOSD neurological function in both NMOSD patients and animal models by increasing CD4⁺Tcm and Treg, reducing of IL-6 and CCL21 level, alleviating spinal cord inflammation and demyelination, and stabilizing astrocytic AQP4 and GFAP expression to minimize neuronal and myelin damage, supporting its clinical utility. Those findings demonstrate LPE’s potential to alleviate acute exacerbations and improve NMOSD management, providing a promising alternative to traditional therapies.