Dataset Information

Differential serum proteomics of neuromyelitis spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD)

ABSTRACT: Neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are two types of autoimmune-mediated central nervous system (CNS) inflammatory demyelinating diseases that have similar clinical manifestations but with different pathogenesis and prognosis. Here we reported on a serum differential proteomic analysis of the patients with the two diseases. Sera of 25 Aquaporin-4 (AQP4)-IgG+ NMOSD patients, 16 MOGAD patients and 8 healthy people were submitted to shotgun analysis using nano-LC-MS/MS. Totally 584 non-redundant proteins were identified, among which 340 proteins were detected in at least three samples per group. Statistical analysis revealed 40 proteins have significant difference in at least one pair-comparison (fold change >=1.2 or <=0.83 and multi-sample test ANOVA-q <0.05). Further, 38 proteins were detected only in the patient groups and not in the healthy control group. Bioinformatic analysis on these 78 proteins revealed that disturbance on immune system, hemostasis processes and carbohydrate metabolism occurred in both diseases, but with different mechanisms. We believe this work could provide useful information to improve the understanding of the mechanisms of NMOSD and MOGAD and suggest potential diagnostic markers and treatment targets.

ORGANISM(S): Homo Sapiens

SUBMITTER: Ya Jin

PROVIDER: PXD059225 | iProX | Wed Dec 25 00:00:00 GMT 2024

REPOSITORIES: iProX

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Publications

A Differential Proteomic Analysis on Patient Sera with Neuromyelitis Spectrum Disorders (NMOSD) and Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) Suggested Shared and Distinct Disease Mechanisms.

Hu Xuhan X Sun Xiaobo X Yang Tingting T Sun Xiaoou X Wen Meiling M Chen Changming C Qiu Wei W Jin Ya Y

Journal of proteome research 20250604 7

Neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are two types of autoimmune-mediated central nervous system (CNS) inflammatory demyelinating diseases that have similar clinical manifestations but with different pathogenesis and prognosis. Here, we reported on a differential proteomic analysis on the patient sera with the two diseases. Serum samples of 25 aquaporin-4 (AQP4)-IgG+ NMOSD patients, 16 MOGAD patients, and 8 he ...[more]

PMID: 40464632

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Project description:Infiltrating T-lymphocytes from the peripheral blood into the central nervous system (CNS) play a dynamic role in the development of a neurological immune-mediated diseases. HAM/TSP is a chronic progressive inflammatory neurological disorder associated with human T-cell lymphotropic virus type I (HTLV-I) infection. In this chronic myelopathy, virus-infected circulating T-cells infiltrate the CNS and an immune response is initiated against the components of CNS. As the HTLV-I proviral load (PVL) has been used as the best clinical marker for patient diagnostic with HAM/TSP, we hypothesized there might be a signature on T-cell receptor (TCR) clonal repertoire in these patients, which could distinguish HAM/TSP patients from the healthy population, as well as from patients with a more heterogeneous CNS-reactive inflammatory disease as multiple sclerosis (MS). With this in mind, we applied an innovative unbiased molecular technique – unique molecular identifier (UMI) library-strategy to investigate with high accuracy the TCR clonal repertoire by high throughput sequencing (HTS) technology. cDNA-TCR β-chain libraries were sequenced from 2 million peripheral mononuclear cells (PBMCs) in 14 HAM/TSP patients, 34 MS patients and 20 healthy controls (HC). To address whether the clonal expansion correlates with the patient’s PVL level, analysis of longitudinal TCR repertoire was performed in 2 HAM/TSP patients. Over 5.6 million TCR sequences were generated per sample on HiSeq 2500 Illumina system and analyzed through the molecular identifier groups-based error correction pipeline (MiGEC). Bioinformatic analysis showed that clones with more than 8 reads had a lower coefficient of variation (CV) and then could be used with confidence to evaluate the TCR clonal expansion. While HAM/TSP patients showed the higher clonal T-cell expansion compared to MS and HC, increase of the TCR clonal expansion was inversely correlated with the diversity of TCR repertoire in all subject’s group. In addition, correlation of the PVL with TCR clonal expansion was observed in HAM/TSP patients at longitudinal time-points. Surprisingly, MS patients showed a higher diversity of TCR repertoire along with a very slight clonal T-cell expansion in comparison to either HAM/TSP patients or HC. Despite of the higher TCR clonal expansion in HAM/TSP patients, a non-shared or “private” TCR repertoire was observed in these patients. No clones that shared the same CDR3 amino acid sequences were seen in HC and MS patients. However, a cluster of related CDR3 amino acid sequences were observed for 18 out of 34 MS patients when evaluated by phylogenetic tree analysis. It suggestes that a TCR-repertoire signature might characterize patients with MS. Our findings suggest that even though a unique TCR-b repertoire shapes the immune response in patients with neurological immune-mediated disease, a relatedness on clonal T-cell repertoire exist in MS.

Dataset Information

Differential serum proteomics of neuromyelitis spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD)

Publications

A Differential Proteomic Analysis on Patient Sera with Neuromyelitis Spectrum Disorders (NMOSD) and Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) Suggested Shared and Distinct Disease Mechanisms.

Similar Datasets

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