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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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Serum 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\n                      <jats:italic>MASP1<\/jats:italic>\n                      and\n                      <jats:italic>MASP2<\/jats:italic>\n                      genes were analysed for associations with MASP\/MAP levels and SLE manifestations.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Patients 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)\u2009to 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)\u2009to 0.56 (95% CI 0.31 to 1.0)). Serum MAP-1 levels correlated with type I interferon activity (Spearman\u2019s rho 0.34, p&lt;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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>These 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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/lupus-2025-001890","type":"journal-article","created":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T16:15:20Z","timestamp":1775751320000},"page":"e001890","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Lectin pathway of complement in SLE: MAP-1 as a marker of haematological manifestations and elevated type I interferon activity"],"prefix":"10.1136","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3654-8874","authenticated-orcid":false,"given":"Linnea","family":"Lindel\u00f6f","sequence":"first","affiliation":[{"name":"Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Garred","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mun-Gwan","family":"Hong","sequence":"additional","affiliation":[{"name":"National Bioinformatics Infrastructure Sweden, Department of Biochemistry and Biophysics, Stockholm University, Science for Life Laboratory, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-1378-9591","authenticated-orcid":false,"given":"Sasha","family":"Wahl V\u00e6lum","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lotte","family":"Holten Petersen","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, University Hospital of Copenhagen, Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6275-7282","authenticated-orcid":false,"given":"Dag","family":"Leonard","sequence":"additional","affiliation":[{"name":"Department of Medical Sciences, Rheumatology, Uppsala University, Uppsala, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ahmed","family":"Sayadi","sequence":"additional","affiliation":[{"name":"Department of Medical Sciences, Rheumatology, Uppsala University, Uppsala, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1834-2688","authenticated-orcid":false,"given":"Vilija","family":"Oke","sequence":"additional","affiliation":[{"name":"Rheumatology Unit, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden"},{"name":"Academic Specialist Center, Center for Rheumatology, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3532-6660","authenticated-orcid":false,"given":"Timothy B","family":"Niewold","sequence":"additional","affiliation":[{"name":"Barbara Volcker Center for Women and Rheumatic Diseases, Hospital for Special Surgery, New York City, New York, 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