S100A9 Differentially Modifies Phenotypic States of Neutrophils, Macrophages, and Dendritic Cells | Zendy

Michelle M. Averill | Zendy; Shelley Barnhart | Zendy; Lev Becker | Zendy; Xin Li | Zendy; Jay W. Heinecke | Zendy; Renee Leboeuf | Zendy; Jessica A. Hamerman | Zendy; Clemens Sorg | Zendy; Claus Kerkhoff | Zendy; Karin Bornfeldt | Zendy

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S100A9 Differentially Modifies Phenotypic States of Neutrophils, Macrophages, and Dendritic Cells

Author(s) -

Michelle M. Averill,

Shelley Barnhart,

Lev Becker,

Xin Li,

Jay W. Heinecke,

Renee Leboeuf,

Jessica A. Hamerman,

Clemens Sorg,

Claus Kerkhoff,

Karin Bornfeldt

Publication year - 2011

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.110.985523

Subject(s) - s100a9 , bone marrow , medicine , immunology , myeloid , inflammation , dendritic cell , microglia , immune system , biology , microbiology and biotechnology , cancer research

S100A9 is constitutively expressed in neutrophils, dendritic cells, and monocytes; is associated with acute and chronic inflammatory conditions; and is implicated in obesity and cardiovascular disease in humans. Most of the constitutively secreted S100A9 is derived from myeloid cells. A recent report demonstrated that mice deficient in S100A9 exhibit reduced atherosclerosis compared with controls and suggested that this effect was due in large part to loss of S100A9 in bone marrow-derived cells.

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