Evidence map›Paper›PMID 41956715›Full record

ArticleLupus science & medicine2026

Lectin pathway of complement in SLE: MAP-1 as a marker of haematological manifestations and elevated type I interferon activity.

Linnea Lindelöf, Peter Garred, Mun-Gwan Hong, Sasha Wahl Vælum, Lotte Holten Petersen, Dag Leonard, Ahmed Sayadi, Vilija Oke, Timothy B Niewold, Lina-Marcela Diaz-Gallo and 4 more

Abstract read
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Article in Lupus science & medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

14 authors.

Linnea LindelöfDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden.ORCID 0000-0002-3654-8874
Peter GarredLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark.
Mun-Gwan HongNational Bioinformatics Infrastructure Sweden, Department of Biochemistry and Biophysics, Stockholm University, Science for Life Laboratory, Stockholm, Sweden.
Sasha Wahl VælumLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark.ORCID 0009-0006-1378-9591
Lotte Holten PetersenLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark.
Dag LeonardDepartment of Medical Sciences, Rheumatology, Uppsala University, Uppsala, Sweden.ORCID 0000-0002-6275-7282
Ahmed SayadiDepartment of Medical Sciences, Rheumatology, Uppsala University, Uppsala, Sweden.
Vilija OkeRheumatology Unit, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0002-1834-2688
Timothy B NiewoldBarbara Volcker Center for Women and Rheumatic Diseases, Hospital for Special Surgery, New York City, New York, USA.ORCID 0000-0003-3532-6660
Lina-Marcela Diaz-GalloRheumatology Unit, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0002-5688-0102
Saedis SaevarsdottirFaculty of Medicine, School of Health Sciences, University of Iceland, Reykjavík, Iceland.
Iva GunnarssonRheumatology Unit, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0002-4514-7706
Elisabet SvenungssonRheumatology Unit, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.ORCID 0000-0003-3396-3244
Oskar ErikssonDepartment of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden oskar.eriksson@igp.uu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSLE is a systemic autoimmune disease in which the complement system plays a key pathogenic role, yet the contribution of the lectin pathway remains unclear. Lectin pathway-dependent complement activation is initiated by pattern-recognition molecules complexed with mannose-binding lectin (MBL)-associated serine proteases (MASPs) and MBL-associated proteins (MAPs). Here, we combined biochemical and genetic analyses to explore associations between MASP/MAP proteins, SLE manifestations and autoantibody specificities.

methodsSerum concentrations of MASP-3, MAP-1 and MASP-2 were measured using ELISA in Swedish patients with SLE (n=522) and population-based matched controls (n=322). Serum type I interferon activity was measured by a cell-based reporter assay. Associations with SLE manifestations and autoantibodies were explored using logistic regression models. Single-nucleotide genetic variants spanning the

resultsPatients with MAP-1 serum concentrations in the highest quartile had significantly higher rates of discoid rash (OR 2.8 (95% CI 1.4 to 5.7)), haematological manifestations (OR 2.1 (95% CI 1.1 to 3.7)) and autoantibodies against Sm, RNP, SSA and SSB (ORs 2.4 (95% CI 1.3 to 4.6) to 3.6 (95% CI 1.7 to 7.7)). Patients in the highest quartiles of MAP-1 and MASP-2 had lower rates of anti-β2GP1 and anti-cardiolipin IgG and IgA anti-phospholipid antibodies (ORs 0.29 (95% CI 0.12 to 0.68) to 0.56 (95% CI 0.31 to 1.0)). Serum MAP-1 levels correlated with type I interferon activity (Spearman's rho 0.34, p<0.0001), which mediated the associations of MAP-1 with haematological manifestations and Sm/RNP autoantibodies. Significant protein quantitative trait loci for MAP-1 and MASP-2 were identified; however, these did not show consistent associations with SLE or specific SLE manifestations.

conclusionsThese results demonstrate a distinct clinical and serological SLE profile associated with components of the lectin pathway. The lectin pathway-regulatory protein MAP-1 displayed the strongest associations and may serve as a marker of SLE manifestations with a type I interferon signature.

Indexed as

Complement Pathway, Mannose-Binding LectinInterferon Type ILupus Erythematosus, SystemicMannose-Binding Protein-Associated Serine ProteasesAdultAutoantibodiesBiomarkersCase-Control StudiesFemaleHumansMaleMiddle AgedPolymorphism, Single NucleotideSwedenAutoantibodiesBiomarkersInterferon Type IMannose-Binding Protein-Associated Serine ProteasesMASP1 protein, humanMASP2 protein, humanAutoantibodiesInflammationLupus Erythematosus, Systemic

Identifiers

PMID41956715
PMCPMC13084892

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