Lupus science & medicine · 2026
Stage-resolved mapping of RP105 (CD180)-negative B cells reveals residual plasmablast-lineage skewing in SLE: a cross-sectional study.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Kanagawa Ayana, Maruyama Akihito, Shibuta Tatsuki, Akahoshi Mitsuteru, Soejima Sachiko, Tada Yoshifumi, Koarada Syuichi
Аннотация
OBJECTIVE: To determine whether clinically inactive/low-activity SLE reflects immunological remission in this cross-sectional study using CD180 (RP105)-anchored, stage-resolved profiling of peripheral B-cell differentiation.
METHODS: CD19+ B cells were analysed by flow cytometry in healthy controls (HCs; n=27), active SLE (n=29; sampled on admission before treatment initiation/escalation) and inactive/low-activity SLE (n=14; biological-free; ≥5 years of sustained Lupus Low Disease Activity State and/or Definition of Remission in SLE remission). Six ordered stages (subsets 0-5) were defined along the CD180-loss trajectory. CXCR5, CD11c, B-cell activating factor receptor and B-cell maturation antigen (BCMA) were quantified. Non-parametric tests with Benjamini-Hochberg false discovery rate (FDR) adjustment were applied.
RESULTS: Active SLE redistributed towards downstream CD180- plasmablast-lineage stages (subsets 2-5) (14.07% vs 1.92% in HCs). Inactive/low-activity SLE retained a residual plasmablast-lineage (subset 2-5: 6.17%) expansion above HC levels despite durable quiescence. In HCs, CXCR5 positivity was high in upstream CD180+ compartments and declined stepwise across the trajectory. CXCR5 positivity at subset 0 was reduced in active SLE (FDR-adjusted p=0.0273) and inactive/low-activity SLE (FDR-adjusted p=0.0015) and at subset 3 in active SLE (FDR-adjusted p=0.0273) versus HCs. CD11c was enriched in upstream compartments during active disease, whereas BCMA was increased in mature downstream CD180- stages.
CONCLUSIONS: CD180-anchored, stage-resolved profiling indicates that clinical quiescence may not fully equate to immunological normalisation in SLE. These cross-sectional observations do not establish durable persistence, and longitudinal validation is needed. An upstream CXCR5 decrement detectable even in long-term quiescence is consistent with extrafollicular-leaning priming changes arising before CD180 loss; however, any implications for longitudinal immunomonitoring remain hypothesis-generating.
METHODS: CD19+ B cells were analysed by flow cytometry in healthy controls (HCs; n=27), active SLE (n=29; sampled on admission before treatment initiation/escalation) and inactive/low-activity SLE (n=14; biological-free; ≥5 years of sustained Lupus Low Disease Activity State and/or Definition of Remission in SLE remission). Six ordered stages (subsets 0-5) were defined along the CD180-loss trajectory. CXCR5, CD11c, B-cell activating factor receptor and B-cell maturation antigen (BCMA) were quantified. Non-parametric tests with Benjamini-Hochberg false discovery rate (FDR) adjustment were applied.
RESULTS: Active SLE redistributed towards downstream CD180- plasmablast-lineage stages (subsets 2-5) (14.07% vs 1.92% in HCs). Inactive/low-activity SLE retained a residual plasmablast-lineage (subset 2-5: 6.17%) expansion above HC levels despite durable quiescence. In HCs, CXCR5 positivity was high in upstream CD180+ compartments and declined stepwise across the trajectory. CXCR5 positivity at subset 0 was reduced in active SLE (FDR-adjusted p=0.0273) and inactive/low-activity SLE (FDR-adjusted p=0.0015) and at subset 3 in active SLE (FDR-adjusted p=0.0273) versus HCs. CD11c was enriched in upstream compartments during active disease, whereas BCMA was increased in mature downstream CD180- stages.
CONCLUSIONS: CD180-anchored, stage-resolved profiling indicates that clinical quiescence may not fully equate to immunological normalisation in SLE. These cross-sectional observations do not establish durable persistence, and longitudinal validation is needed. An upstream CXCR5 decrement detectable even in long-term quiescence is consistent with extrafollicular-leaning priming changes arising before CD180 loss; however, any implications for longitudinal immunomonitoring remain hypothesis-generating.