{"entity": "researcher", "timestamp": "2026-04-15T18:42:11.195Z", "family": "Niewold", "given": "Timothy B", "initials": "TB", "orcid": "0000-0003-3532-6660", "affiliations": ["Barbara Volcker Center for Women and Rheumatic Diseases, Hospital for Special Surgery, New York City, New York, USA."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/89b178dc1ef34fa4b4ef34e71b9ac1e5.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/89b178dc1ef34fa4b4ef34e71b9ac1e5"}}, "publications": [{"entity": "publication", "iuid": "8be8d00d65424632a6066715fa2207b8", "links": {"self": {"href": "https://publications.scilifelab.se/publication/8be8d00d65424632a6066715fa2207b8.json"}, "display": {"href": "https://publications.scilifelab.se/publication/8be8d00d65424632a6066715fa2207b8"}}, "title": "Lectin pathway of complement in SLE: MAP-1 as a marker of haematological manifestations and elevated type I interferon activity.", "authors": [{"family": "Lindel\u00f6f", "given": "Linnea", "initials": "L", "orcid": "0000-0002-3654-8874", "researcher": {"href": "https://publications.scilifelab.se/researcher/65f6c8233c5547f2885b3e55bbec2601.json"}}, {"family": "Garred", "given": "Peter", "initials": "P"}, {"family": "Hong", "given": "Mun-Gwan", "initials": "MG"}, {"family": "Wahl V\u00e6lum", "given": "Sasha", "initials": "S", "orcid": "0009-0006-1378-9591", "researcher": {"href": "https://publications.scilifelab.se/researcher/6668483bc5d1464f839e525848a5b84c.json"}}, {"family": "Holten Petersen", "given": "Lotte", "initials": "L"}, {"family": "Leonard", "given": "Dag", "initials": "D", "orcid": "0000-0002-6275-7282", "researcher": {"href": "https://publications.scilifelab.se/researcher/42ed25c2f495484db4757f4fef51abae.json"}}, {"family": "Sayadi", "given": "Ahmed", "initials": "A"}, {"family": "Oke", "given": "Vilija", "initials": "V", "orcid": "0000-0002-1834-2688", "researcher": {"href": "https://publications.scilifelab.se/researcher/c5115e955050467694c2e2396706066a.json"}}, {"family": "Niewold", "given": "Timothy B", "initials": "TB", "orcid": "0000-0003-3532-6660", "researcher": {"href": "https://publications.scilifelab.se/researcher/89b178dc1ef34fa4b4ef34e71b9ac1e5.json"}}, {"family": "Diaz-Gallo", "given": "Lina-Marcela", "initials": "LM", "orcid": "0000-0002-5688-0102", "researcher": {"href": "https://publications.scilifelab.se/researcher/7fc169ccfb154ef29c62f78044e27a7b.json"}}, {"family": "Saevarsdottir", "given": "Saedis", "initials": "S"}, {"family": "Gunnarsson", "given": "Iva", "initials": "I", "orcid": "0000-0002-4514-7706", "researcher": {"href": "https://publications.scilifelab.se/researcher/90121ddba7fe4f928c1b121b162c2509.json"}}, {"family": "Svenungsson", "given": "Elisabet", "initials": "E", "orcid": "0000-0003-3396-3244", "researcher": {"href": "https://publications.scilifelab.se/researcher/0ab5989c3c604a96bf42b1b6f90434a0.json"}}, {"family": "Eriksson", "given": "Oskar", "initials": "O"}], "type": "journal article", "published": "2026-04-09", "journal": {"title": "Lupus Sci Med", "issn": "2053-8790", "volume": "13", "issue": "1", "issn-l": "2053-8790"}, "abstract": "SLE 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.\n\nSerum 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 MASP1 and MASP2 genes were analysed for associations with MASP/MAP levels and SLE manifestations.\n\nPatients 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-\u03b22GP1 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.\n\nThese 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.", "doi": "10.1136/lupus-2025-001890", "pmid": "41956715", "labels": {"Bioinformatics (NBIS)": "Collaborative", "Bioinformatics Support and Infrastructure": "Collaborative", "Bioinformatics Support, Infrastructure and Training": "Collaborative"}, "xrefs": [{"db": "pii", "key": "13/1/e001890"}], "notes": [], "created": "2026-04-15T06:40:16.897Z", "modified": "2026-04-15T06:40:17.508Z"}]}