Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS
In this study, researchers analyzed cerebrospinal fluid (CSF) cytokines and complement components in people with AQP4+ NMOSD, MOGAD, and MS showing recent disease activity. They found elevated CSF IL-10 and TNF-a in all groups, with specific elevations of IL-6 in AQP4+ NMOSD and MOGAD. Notably, certain complement activation products were uniquely elevated in MS. Correlations were observed between biomarkers like GFAP, NfL and various cytokines/complement components.
- Tags
- #MSResearch
- Most relevant to
- —
- Human efficacy
- Not established from this source
- Mechanism
- Not reported
- Evidence strength
- Not graded
- Outcome
- Not reported
Why it matters
This research highlights distinct CSF cytokine and complement profiles in neuroinflammatory diseases, supporting a better understanding of disease mechanisms and potentially guiding future diagnostic approaches. It enhances the knowledge of inflammation in MS and related diseases.
What this does not prove
The study suggests potential differences in immune profiling among neuroinflammatory diseases but emphasizes the need for validation in larger cohorts before any concrete conclusions can be drawn.
Next milestone
No next milestone was established from the available source.
Study facts
- Study design
- Not reported
- Participants / samples
- Not reported
- Randomised
- Not reported
- Controlled
- Not reported
- Primary endpoint met
- Not reported
- Relevant MS type
- Not reported
- Publication date
- 2026-10-21
- Evidence reviewed
- Abstract only
- Regulatory approval
- Not reported
- Research areas
- Not classified
- Biological target
- C2b, C3d, C4a, C5a
- Pathway
- Not reported
- Population
- People with recent disease activity in MS (n=36)
- Size of effect
- Not reported
- Secondary endpoints
- Not reported
- MRI endpoints
- Not reported
- Biomarkers
- NfL; GFAP
- Safety
- Not reported
Original sources
- Primary evidenceInvestigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS. ↗DOI: 10.1002/acn3.70549
Supporting passages (9)
publication datePublication date: 2026-10-21
comparatorControls included subjects with non-inflammatory conditions (CSF: n = 51) and healthy controls (plasma: n = 29).
biological targetsMost complement components were elevated in AQP4+ NMOSD and MOGAD; only specific activation products (C2b, C3d, C4a, C5a) were elevated in MS.
populationMETHODS: CSF complement components, CSF and plasma cytokines, neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) were measured in people with AQP4+ NMOSD (CSF: n = 19; plasma: n = 18), MOGAD (CSF: n = 29; plasma: n = 35) and MS (CSF: n = 36; plasma: n = 58) with recent disease activity.
biomarkersCSF GFAP and NfL correlated with several CSF cytokines and complement components in AQP4+ NMOSD and MOGAD.
findingsRESULTS: CSF IL-10 and TNF-a were elevated across all neuroinflammatory disease groups relative to controls. CSF IL-6 was elevated only in AQP4+ NMOSD and MOGAD. There were no significant differences in plasma cytokines between groups. Most complement components were elevated in AQP4+ NMOSD and MOGAD; only specific activation products (C2b, C3d, C4a, C5a) were elevated in MS. CSF GFAP and NfL correlated with several CSF cytokines and complement components in AQP4+ NMOSD and MOGAD. Expanded Disability Status Scale at nadir during attacks correlated with CSF BAFF, GFAP, free C1q, C1s, C1s-C1inh, C4a in AQP4+ NMOSD, and CSF IL-10, TNF-a, free C1q, C1inh, C4a in MOGAD.
limitationsTitle: Investigation of Complement Activation and Cytokine Signatures in AQP4+ NMOSD, MOGAD, and MS.
peer reviewedPublication types: Journal Article
subjectsMETHODS: CSF complement components, CSF and plasma cytokines, neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) were measured in people with AQP4+ NMOSD (CSF: n = 19; plasma: n = 18), MOGAD (CSF: n = 29; plasma: n = 35) and MS (CSF: n = 36; plasma: n = 58) with recent disease activity.
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