Our review article discusses the relationship between systemic lupus erythematosus and the mannose-binding lectin gene. The complex trait of systemic lupus erythematosus (SLE), which manifests as a variety of clinical phenotypes and the production of several autoantibodies, is SLE. SLE patients experience a wide range of clinical phenotypes, such as skin rash, and neuropsychiatric, and musculoskeletal symptoms, some of which can progress to lupus nephritis. Abnormal complement activation causes inflammation, which damages multiple organs' tissue. About 50% of systemic lupus erythematosus patients, a chronic inflammatory disease, experience kidney damage. Despite effective anti-inflammatory and immunosuppressive therapies, lupus nephritis still results in end-stage kidney impairment (ESRD) or chronic kidney disorder (CKD) for an excessive number of patients. It represents a significant risk factor regarding mortality and morbidity in SLE. The family of C-type lectins of collectins includes the mannose-binding lectin (MBL), whose portion in the pre-immune first line of defense seems to involve pattern recognition. MBL can identify carbohydrate modes that abound on the surfaces of numerous pathogenic bacterial, viral, protozoal, and fungal microorganisms. The complement system's lectin pathway is activated when MBL binds to a microorganism. Numerous studies have linked MBL polymorphism, SLE, and lupus nephritis.