Pathogenic B-T Cell Axis Driven by BAFF Induces Endothelial Apoptosis in SLE-PAH.

Circulation Research · 23 Oct 2026 · Journal Article

Jiang, Ma + more

The abstract is read at the publisher; the summary is JClub's.

BAFF is significantly upregulated in SLE-PAH, and BAFF overexpression in humanized BAFF-transgenic mice drives a S100a6+ mature B-cell subset that triggers endothelial apoptosis and pulmonary vascular remodeling.

Why it matters: The mechanisms linking SLE autoimmune dysregulation to fatal PAH progression are poorly defined, limiting effective therapies for SLE-PAH.
What they did: The study measured BAFF in SLE-PAH patients and animal models, then used single-cell RNA sequencing, flow cytometry, histology, and cell-based assays in humanized BAFF-transgenic mice; Belimumab was tested in two SLE-PAH animal models.
The result: Belimumab neutralization ameliorated autoimmune and cardiopulmonary manifestations and improved survival in both animal models, supporting BAFF inhibition as a therapeutic strategy for SLE-PAH.

AI summary of the abstract · may contain errors · not medical advice · read the paper.

1 cites

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bioRxiv · 1 Nov 2026 · Preprint
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Pathogenic B-T Cell Axis Driven by BAFF Induces Endothelial Apoptosis in SLE-PAH.

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Dynamic effects of fructose and Momordica charantia supplementation on pulmonary hypertension in broiler chickens

Multimodality Molecular Profiling Nominates Targetable Mechanisms in Progressive RV Dysfunction.

EBF1 controls an embryonic artery-forming niche that reactivates in pulmonary arterial hypertension

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