Treatment of monocytes with interleukin (IL)‐12 plus IL‐18 stimulates survival, differentiation and the production of CXC chemokine ligands (CXCL)8, CXCL9 and CXCL10

• Published in: Clinical and experimental immunology 2006-09, Vol.145 (3), p.535-544
• Main Authors: Coma, G., Peña, R., Blanco, J., Rosell, A., Borras, F. E., Esté, J. A., Clotet, B., Ruiz, L., Parkhouse, R. M. E., Bofill, M.
• Format: Article
• Language: English
• Subjects: Analysis of Variance; angiogenic chemokines; Basic Immunology; Biological and medical sciences; bronchoalveolar macrophages; Cell Differentiation - drug effects; Cell Survival - drug effects; Cells, Cultured; Chemokine CXCL10; Chemokine CXCL9; Chemokines, CXC - biosynthesis; cytokines; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; IL‐12; IL‐18; Immunity, Innate; Immunopathology; innate immunity; Interleukin-12 - pharmacology; Interleukin-18 - pharmacology; Interleukin-8; Macrophages, Alveolar - immunology; Medical sciences; monocytes; Monocytes - immunology; Phagocytosis; STAT4 Transcription Factor - analysis; Stimulation, Chemical
• ISSN: 0009-9104; 1365-2249
• DOI: 10.1111/j.1365-2249.2006.03145.x

Summary During inflammation, interleukin (IL)‐12 and IL‐18 are produced by macrophages and other cell types such as neutrophils (IL‐12), keratinocytes and damaged endothelial cells (IL‐18). To explore the role of IL‐12 and IL‐18 in inflammatory innate immune responses we investigated their impact on human peripheral blood monocytes and mature bronchoalveolar lavage (BAL) macrophages. IL‐12 and IL‐18 together, but not alone, prevented spontaneous apoptosis of cultured monocytes, promoted monocyte clustering and subsequent differentiation into macrophages. These morphological changes were accompanied by increased secretion of CXC chemokine ligands (CXCL)9, CXCL10 (up to 100‐fold, P