Dataset Information

Data in support of Precision Proteomic Profiling of Systemic Lupus Erythematosus

ABSTRACT: In this study, we aimed to investigate the molecular basis for patient subtyping to form the basis for clinical differentiation of SLE patients with high versus low levels of C3dg as well as high versus low SLEDAI scores. Our study applied primarily applied a high-throughput LC-MS/MS method capable of analyzing 500 samples per day (SPD) , global assessment of autoantibody profiles as well as inflammatory markers. The ob-jective of this study is to investigate the biological processes associated with these two measures, and to determine whether these markers reflect overlapping or distinct bi-ological processes.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

DISEASE(S): Systemic Lupus Erythematosus

SUBMITTER: Allan Stensballe

LAB HEAD: Allan Stensballe

PROVIDER: PXD066214 | Pride | 2026-06-29

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	500SPD-Lupus_Allan-digest_10B.timeseries.data	Other
	500SPD-Lupus_Allan-digest_10B.wiff	Wiff
	500SPD-Lupus_Allan-digest_10B.wiff.scan	Wiff
	500SPD-Lupus_Allan-digest_10B.wiff2	Wiff
	500SPD-Lupus_Allan-digest_10C.timeseries.data	Other

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Publications

Precision Proteomic Profiling of Systemic Lupus Erythematosus-Correlating Disease Activity and Complement Levels with Clinical Phenotypes.

Skallerup Jacob J Aboo Christopher C Bekker-Jensen Dorte B DB Tran Katherine K Ren Jie J Jørgensen Malene Møller MM Blackburn Jonathan M JM Troldborg Anne A Stensballe Allan A

Biomedicines 20260622 6

<b>Background/Objectives:</b> Systemic lupus erythematosus (SLE) is characterized by diverse clinical presentations and complex immunological mechanisms. This study aimed to characterize patient serology associated with disease activity scored using the systemic lupus erythematosus disease activity index (SLEDAI) and investigate the molecular signature of complement activation (measured through C3dg, a complement breakdown product) in SLE patients utilizing high-throughput mass spectrometry and ...[more]

PMID: 42351836

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Project description:Abstract Background Vertebral endplate signal intensity changes visualized by magnetic resonance imaging termed Modic changes (MC) are highly prevalent in low back pain patients. Interconvertibility between the three MC subtypes (MC1, MC2, MC3) suggests different pathological stages. Histologically, granulation tissue, fibrosis, and bone marrow edema are signs of inflammation in MC1 and MC2. However, different inflammatory infiltrates and amount of fatty marrow suggest distinct inflammatory processes in MC2. Aims The aims of this study were to investigate i) the degree of bony (BEP) and cartilage endplate (CEP) degeneration in MC2, ii) to identify inflammatory MC2 pathomechanisms, and iii) to show that these marrow changes correlate with severity of endplate degeneration. Methods Pairs of axial biopsies (n=58) spanning the entire vertebral body including both CEPs were collected from human cadaveric vertebrae with MC2. From one biopsy, the bone marrow directly adjacent to the CEP was analyzed with mass spectrometry. Differentially expressed proteins (DEPs) between MC2 were identified and bioinformatic enrichment analysis was performed. The other biopsy was processed for paraffin histology and BEP/CEP degenerations were scored. Endplate scores were correlated with DEPs. Results Endplates from MC2 were significantly more degenerated. Proteomic analysis revealed an activated complement system, increased expression of extracellular matrix proteins, angiogenic, and neurogenic factors in MC2 marrow. Endplate scores correlated with upregulated complement and neurogenic proteins. Discussion The inflammatory pathomechanisms in MC2 comprises activation of the complement system. Concurrent inflammation, fibrosis, angiogenesis, and neurogenesis indicate that MC2 is a chronic inflammation. Correlation of endplate damage with complement and neurogenic proteins suggest that complement system activation and neoinnervation may be linked to endplate damage. The endplate-near marrow is the pathomechanistic site, because MC2 occur at locations with more endplate degeneration. Conclusion MC2 are fibroinflammatory changes with complement system involvement which occur adjacent to damaged endplates.