SR-A1 cooperates with TLR4-NF-κB signaling to drive macrophage TGF-β1 expression and Treg induction during schistosome infection.

SR-A1 cooperates with TLR4 signaling in macrophages to enhance TGF-β1 expression, assembling c-Jun–p50 complexes at the Tgfb1 promoter during Schistosoma japonicum infection.

• Why it matters: Helminths induce Tregs to sustain chronic infection, and TGF-β1 is essential for Foxp3-driven Treg induction, but how helminths trigger macrophage TGF-β1 production is unclear.
• What they did: In Schistosoma japonicum-infected mice, schistosome egg antigens activate TLR4–p50 (NF-κB1) and engage SR-A1 to upregulate c-Jun, promoting c-Jun–p50 transcription complexes at the Tgfb1 promoter.
• The result: This SR-A1–TLR4 cooperation increases macrophage TGF-β1, induces Tregs, and mitigates liver immunopathology in Schistosoma japonicum-infected mice, suggesting a therapeutic target for inflammatory helminthiasis.

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