TLR stimulation initiates a CD39-based autoregulatory mechanism that limits macrophage inflammatory responses

Author:

Cohen Heather B.12,Briggs Katharine T.3,Marino John P.34,Ravid Katya5,Robson Simon C.6,Mosser David M.12

Affiliation:

1. Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD;

2. Maryland Pathogen Research Institute, College Park, MD;

3. Institute for Bioscience and Biotechnology Research, Rockville, MD;

4. National Institute of Standards and Technology, Rockville, MD;

5. Department of Biochemistry, School of Medicine, Boston University, Boston, MA; and

6. Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA

Abstract

Key Points TLR-stimulated macrophages synthesize, release, and hydrolyze ATP via CD39 to regulate their own activation state. The loss of macrophage CD39 prevents regulatory macrophage development and leads to lethal inflammatory responses and septic shock in mice.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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