Immunity：陈列平/王俊合作发现系统性红斑狼疮等自身免疫疾病治疗新靶点
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TL;DR - A Yale (Chen Lieping) / NYU (Wang Jun) collaboration published in Immunity (July 30, 2026) reports that the liver-secreted protein FGL1 acts as an inhibitory ligand for the B-cell receptor TACI, revealing a druggable checkpoint for B-cell–driven autoimmunity such as systemic lupus erythematosus (SLE). Note: the article describes wet-lab immunology with no AI/ML component, despite the digest's AI framing.
- FGL1 was previously known only as a ligand for the T-cell co-inhibitory receptor LAG3; a genome-wide cell-surface proteome screen identified TACI (a TNFR-family receptor for BAFF/APRIL) as a second FGL1 receptor.
- FGL1 binds TACI at an N-terminal site distinct from the BAFF/APRIL binding region and drives TACI internalization, reducing receptor availability for activating ligands and restraining an innate-like B-cell subset.
- Recombinant FGL1 reduced antigen-specific IgM responses, B-cell numbers, and autoimmune symptoms in B6/lpr lupus-like mice; the effect was abolished in Taci-/- mice, establishing receptor dependence.
- Therapeutic implication: targeting FGL1–TACI could selectively dampen B-cell activation without full B-cell depletion (e.g., CAR-T or broad immunosuppression), potentially lowering infection risk.
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Immunity：陈列平/王俊合作发现系统性红斑狼疮等自身免疫疾病治疗新靶点
TL;DR - A Yale (Chen Lieping) / NYU (Wang Jun) collaboration published in Immunity (July 30, 2026) reports that the liver-secreted protein FGL1 acts as an inhibitory ligand for the B-cell receptor TACI, revealing a druggable checkpoint for B-cell–driven autoimmunity such as systemic lupus erythematosus (SLE). Note: the article describes wet-lab immunology with no AI/ML component, despite the digest's AI framing.
- FGL1 was previously known only as a ligand for the T-cell co-inhibitory receptor LAG3; a genome-wide cell-surface proteome screen identified TACI (a TNFR-family receptor for BAFF/APRIL) as a second FGL1 receptor.
- FGL1 binds TACI at an N-terminal site distinct from the BAFF/APRIL binding region and drives TACI internalization, reducing receptor availability for activating ligands and restraining an innate-like B-cell subset.
- Recombinant FGL1 reduced antigen-specific IgM responses, B-cell numbers, and autoimmune symptoms in B6/lpr lupus-like mice; the effect was abolished in Taci-/- mice, establishing receptor dependence.
- Therapeutic implication: targeting FGL1–TACI could selectively dampen B-cell activation without full B-cell depletion (e.g., CAR-T or broad immunosuppression), potentially lowering infection risk.