ArticleProceedings of the National Academy of Sciences of the United States of America2024
Enforced CARD11/MALT1 signaling in dendritic cells triggers hemophagocytic lymphohistiocytosis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Increasing hydrophobicity in poly(amino acid) adjuvants elicits potent and durable anti-tumor immunityBioactive materials · 2027Article
- Decoding Allosteric Inhibition in MALT1: The Hidden Role of Conformational Plasticity in Metastable States via Biased MD and Deep Learning.The journal of physical chemistry. B · 2026Article
- The pathophysiology of hemophagocytic lympho-histiocytosis (HLH) syndrome and insights from animal models.Clinical and experimental immunology · 2025Review
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10 authors.
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Abstract
Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening syndrome fueled by uncontrolled mononuclear phagocyte activity, yet the innate immune mechanisms driving HLH pathogenesis remain elusive. Germline gain-of-function (GOF) mutations in CARD11, a pivotal regulator of lymphocyte antigen receptor signaling, cause the lymphoproliferative disease B-cell expansion with NF-κB and T-cell anergy, which is frequently associated with HLH development. Given that CARD11 is physiologically expressed not only in lymphocytes but also in dendritic cells (DCs), we explored whether enforced CARD11 signaling in DCs contributes to immunopathology. We demonstrated that exclusive DC-intrinsic expression of CARD11-GOF in mice was sufficient to induce a lethal autoinflammatory syndrome that mimicked human HLH. Mechanistically, DC-intrinsic CARD11-GOF signaling triggered cell-autonomous inflammatory cytokine production via MALT1 paracaspase engagement. Genetic deletion of
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