Lupus science & medicine · 2026
Fatigue outcomes with anifrolumab in low-disease-activity SLE: DNA damage in plasmacytoid dendritic cells as a candidate biomarker for responders.
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Yoshida Eitaro, Kuga Taiga, Yanagimoto Yusuke, Nakanishi Emi, Makiyama Ayako, Murayama Goh, Minowa Kentaro, Kusaoi Makio, Yamaji Ken, Tamura Naoto
Аннотация
OBJECTIVE: Investigate the effect of anifrolumab on fatigue in patients with SLE and low disease activity and identify cellular mechanisms associated with the fatigue response.
METHODS: 12 SLE patients with significant fatigue (Fatigue Assessment Scale (FAS)1 ≥22) initiating anifrolumab were followed at baseline, 1 month and 3 months. The primary endpoint was fatigue improvement (FAS reduction ≥4 points). Secondary endpoints included FAS, Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), Generalised Anxiety Disorder-7, Quick Inventory of Depressive Symptomatology Self-Report-16, serum interferon (IFN)-α, type I IFN activity and γH2AX expression in myeloid subsets by flow cytometry.
RESULTS: Median baseline SLEDAI was 4 (IQR 4–7) and median FAS was 28 (IQR 24–36). Fatigue improvement, defined by FAS reduction ≥4 points, was observed in 58% of patients (7/12; 95% CI 29% to 88%) at 3 months. Serum IFN-α was low across the cohort and did not predict response. Baseline γH2AX in plasmacytoid dendritic cells (pDCs) was significantly higher in responders than in non-responders and healthy controls and showed a declining trend after 1 month of treatment (Wilcoxon signed-rank test, n=6, p=0.156).
CONCLUSIONS: These preliminary findings suggest that anifrolumab may improve fatigue in patients with SLE including those with low disease activity and low serum IFN-α. Elevated pDC γH2AX at baseline, reflecting subclinical cellular stress, may identify patients who could benefit from IFN blockade for fatigue. These hypothesis-generating findings warrant validation in controlled studies.
METHODS: 12 SLE patients with significant fatigue (Fatigue Assessment Scale (FAS)1 ≥22) initiating anifrolumab were followed at baseline, 1 month and 3 months. The primary endpoint was fatigue improvement (FAS reduction ≥4 points). Secondary endpoints included FAS, Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), Generalised Anxiety Disorder-7, Quick Inventory of Depressive Symptomatology Self-Report-16, serum interferon (IFN)-α, type I IFN activity and γH2AX expression in myeloid subsets by flow cytometry.
RESULTS: Median baseline SLEDAI was 4 (IQR 4–7) and median FAS was 28 (IQR 24–36). Fatigue improvement, defined by FAS reduction ≥4 points, was observed in 58% of patients (7/12; 95% CI 29% to 88%) at 3 months. Serum IFN-α was low across the cohort and did not predict response. Baseline γH2AX in plasmacytoid dendritic cells (pDCs) was significantly higher in responders than in non-responders and healthy controls and showed a declining trend after 1 month of treatment (Wilcoxon signed-rank test, n=6, p=0.156).
CONCLUSIONS: These preliminary findings suggest that anifrolumab may improve fatigue in patients with SLE including those with low disease activity and low serum IFN-α. Elevated pDC γH2AX at baseline, reflecting subclinical cellular stress, may identify patients who could benefit from IFN blockade for fatigue. These hypothesis-generating findings warrant validation in controlled studies.