The NLRP3 inflammasome functions as a driver of the myelodysplastic syndrome phenotype

Author:

Basiorka Ashley A.1,McGraw Kathy L.2,Eksioglu Erika A.3,Chen Xianghong3,Johnson Joseph4,Zhang Ling5,Zhang Qing2,Irvine Brittany A.2,Cluzeau Thomas6789,Sallman David A.2,Padron Eric2,Komrokji Rami2,Sokol Lubomir2,Coll Rebecca C.10,Robertson Avril A. B.10,Cooper Matthew A.10,Cleveland John L.11,O’Neill Luke A.12,Wei Sheng3,List Alan F.2

Affiliation:

1. Cancer Biology Ph.D. Program, Department of Malignant Hematology,

2. Department of Malignant Hematology,

3. Department of Immunology,

4. Analytic Microscopy Core Facility, and

5. Department of Hematopathology, H. Lee Moffitt Cancer Center, Tampa, FL;

6. Department of Hematology, Centre Hospitalier Universitaire de Nice, Nice, France;

7. Faculty of Medicine, University Nice Sophia Antipolis, Nice, France;

8. INSERM U1065, Mediterranean Center of Molecular Medicine, Nice, France;

9. French Group of Myelodysplasia, Paris, France;

10. Institute for Molecular Bioscience, University of Queensland, Brisbane, Australia;

11. Department of Tumor Biology, H. Lee Moffitt Cancer Center, Tampa, FL; and

12. Trinity Biomedical Sciences Institute, School of Biochemistry and Immunology, Trinity College Dublin, Dublin, Ireland

Abstract

Key Points Key biological features of MDSs are explained by NLRP3 inflammasome activation, which drives pyroptotic cell death and β-catenin activation. Alarmin signals and founder gene mutations license this redox-sensitive inflammasome platform.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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