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Objectives The complement system plays an essential role in the pathogenesis of systemic lupus erythematosus (SLE). We recently demonstrated a link between ficolin-3, and initiator of the lectin pathway of complement, and autoantibody profile in Swedish SLE patients. However, data regarding the role of the lectin pathway in African populations with SLE are totally lacking. We, therefore, investigated the relevance of ficolin-3 activity in a Sudanese SLE cohort.Methods We included 92 Sudanese SLE patients and 100 age and sex matched healthy controls. Ficolin-3 activity was measured in serum using an in-house developed functional ELISA. Circulating immune complexes (CIC), autoantibodies targeting ten ANA specificities, cardiolipin, β2GPI and phosphatidylserine/prothrombin complex in serum along with 72 plasma inflammatory biomarkers were quantified. We also explored associations between ficolin-3 activity and clinical profiles.Results Serum ficolin-3 activity was significantly higher in Sudanese patients with SLE compared to control individuals (p <0.0001). Among the different ANA specificites, only anti-Sm positivity associated with high levels of ficolin-3 (OR [95% CI] = 3.4 [1.1-10.7], p-value 0.034). In contrast, we found a negative association with anti-β2GPI IgG autoantibodies (OR [95% CI] = 0.17 [0.03-0.86], p-value 0.032). Ficolin-3 associated positively with 10 inflammatory plasma proteins, interestingly, strongest with type I IFN-induced chemokines (MCP-3, CCL19, CXCL10; p-value 0.01, 0.01, and 0.02, respectively) and IL-18 (p-value 0.0001). Ficolin-3 also correlated with SLEDAI score, CIC, and negatively with the occurrence of thrombotic and/or obstetric complications.Conclusions The association between ficolin-3 activity and anti-Sm antibodies, IFN-induced chemokines, and SLEDAI indicates a potential role of the lectin pathway in the pathogenesis and severity of SLE in African populations. Possibly, this role is mediated by a type I IFN response. We could also replicate our previous finding, demonstrating a consistent negative association with antiphospholipid antibodies, although this needs further exploration.