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PK1/EG‐VEGF induces monocyte differentiation and activation
Author(s) -
Dorsch Marion,
Qiu Yubin,
Soler Dulce,
Frank Nita,
Duong Thao,
Goodearl Andrew,
O’Neil Steve,
Lora Jose,
Fraser Christopher C.
Publication year - 2005
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0205061
Subject(s) - biology , proinflammatory cytokine , cd14 , chemokine , monocyte , immunology , microbiology and biotechnology , tumor necrosis factor alpha , population , immune system , inflammation , medicine , environmental health
Macrophages exist as sentinels in innate immune response and react by expressing proinflammatory cytokines and up‐regulating antigen‐presenting and costimulatory molecules. We report a novel function for prokineticin‐1 (PK1)/endocrine gland‐derived vascular endothelial growth factor. Screening of murine tissue sections and cells for specific binding site leads to the identification of macrophages as an in vivo cellular target for PK1. We demonstrate PK1 induces differentiation of murine and human bone marrow cells into the monocyte/macrophage lineage. Human peripheral blood monocytes respond to PK1 by morphological changes and down‐regulation of B7‐1, CD14, CC chemokine receptor 5, and CXC chemokine receptor 4. Monocytes treated with PK1 have elevated interleukin (IL)‐12 and tumor necrosis factor α and down‐regulated IL‐10 production in response to lipopolysaccharide. PK1 induces a distinct monocyte‐derived cell population, which is primed for release of proinflammatory cytokines that favor a T helper cell type 1 response.