The Journal of clinical endocrinology and metabolism · 2026
Increased MAP-1 and lectin complement activation capacity in Klinefelter syndrome.
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Chang Simon, Just Jesper, Skakkebæk Anne, Hasselholm Emma B, Nielsen Christian, Garred Peter, Gravholt Claus H, Münster Anna-Marie Bloch, Palarasah Yaseelan
Аннотация
CONTEXT: Klinefelter syndrome (KS) is a congenital condition linked to immune dysregulation and metabolic dysfunction with an increased risk of autoimmune, metabolic, and cardiovascular diseases.
OBJECTIVE: We examined complement activation through the lectin pathway in men with KS and its relationships with hypogonadism, body composition, and fibrinolytic function.
METHODS: We conducted a cross-sectional study comparing men with KS with age-matched controls. We measured lectin pathway complement activation capacity, individual lectin complement factors including the lectin pathway regulator MAP-1, and the main complement split product, C3dg, using ELISAs. Body composition was assessed by dual-energy X-ray absorptiometry, and fibrin clot lysis was analyzed via turbidometry. Additionally, we analyzed skeletal muscle mRNA expression of the MASP1 gene splice variant MASP1-201, which encodes MAP-1.
RESULTS: Lectin pathway activation capacity was higher in 45 men with KS compared to 45 male controls (mean ± SD, 106.2 ± 51.6% vs 64.0 ± 30.1%, P < .0001). Serum MAP-1 levels were also elevated in KS patients. MASP1-201 expression was increased in KS. Serum C3dg levels were not different between KS and controls. The lectin pathway activation capacity was not strongly linked to sex hormone levels and only had a weak association with body fat. The lectin pathway contributed to fibrin clot lysis variability in KS, and levels of the fibrinogen-C3dg complex were similar in both KS and controls.
CONCLUSION: Men with KS demonstrate increased lectin complement pathway activation capacity, and increased MAP-1 and MASP1-201 expression. Altered immune function could be a specific characteristic of KS contributing to the comorbidity burden.
OBJECTIVE: We examined complement activation through the lectin pathway in men with KS and its relationships with hypogonadism, body composition, and fibrinolytic function.
METHODS: We conducted a cross-sectional study comparing men with KS with age-matched controls. We measured lectin pathway complement activation capacity, individual lectin complement factors including the lectin pathway regulator MAP-1, and the main complement split product, C3dg, using ELISAs. Body composition was assessed by dual-energy X-ray absorptiometry, and fibrin clot lysis was analyzed via turbidometry. Additionally, we analyzed skeletal muscle mRNA expression of the MASP1 gene splice variant MASP1-201, which encodes MAP-1.
RESULTS: Lectin pathway activation capacity was higher in 45 men with KS compared to 45 male controls (mean ± SD, 106.2 ± 51.6% vs 64.0 ± 30.1%, P < .0001). Serum MAP-1 levels were also elevated in KS patients. MASP1-201 expression was increased in KS. Serum C3dg levels were not different between KS and controls. The lectin pathway activation capacity was not strongly linked to sex hormone levels and only had a weak association with body fat. The lectin pathway contributed to fibrin clot lysis variability in KS, and levels of the fibrinogen-C3dg complex were similar in both KS and controls.
CONCLUSION: Men with KS demonstrate increased lectin complement pathway activation capacity, and increased MAP-1 and MASP1-201 expression. Altered immune function could be a specific characteristic of KS contributing to the comorbidity burden.