Tumor necrosis factor alpha gene variants do not display allelic imbalance in circulating myeloid cells

• Published in: Cellular immunology Vol. 262; no. 2; pp. 127 - 133
• Main Authors: Wienzek, Sandra, Kissel, Karin, Breithaupt, Kirstin, Lang, Christina, Nockher, Angelika, Hackstein, Holger, Bein, Gregor
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 2010
• Subjects: Adolescent; Adult; Allelic Imbalance; Blood donors; Female; Genetic polymorphism; Genotype; Humans; Lipopolysaccharide Receptors - immunology; Male; Middle Aged; Monocytes - cytology; Monocytes - immunology; Myeloid Cells - cytology; Myeloid Cells - physiology; Neutrophils - cytology; Neutrophils - immunology; Polymorphism, Genetic; Promoter Regions, Genetic - genetics; Prospective Studies; Receptors, IgG - immunology; Risk allele; TNF −308 A/G; Tumor necrosis factor α; Tumor Necrosis Factor-alpha - genetics; Tumor Necrosis Factor-alpha - metabolism; Young Adult; Risk allele; Allelic imbalance; Tumor necrosis factor α; Genetic polymorphism; TNF −308 A/G
• ISSN: 0008-8749; 1090-2163
• DOI: 10.1016/j.cellimm.2010.02.004

Carriage of the TNF −308 A allele (rs1800629 A) has been associated with increased serum TNF-α levels, the development of sepsis syndrome, and fatal outcome, in severely traumatized patients (Menges et al., 2008 [1]). Herein, we analysed the putative allelic imbalance of TNF-α release from myeloid cells. Circulating peripheral blood cells from healthy human blood donors ( n = 104) and monocyte-derived macrophages ( n = 158) were analysed for their ex vivo capacity of TNF-α expression. Our findings indicate that carriage of the TNF −308 A allele is not associated with high TNF-α expression in circulating human leucocytes and monocyte-derived macrophages. Other cellular sources, e.g. tissue-resident cells like mast cells and/or tissue specific macrophages might be the cellular source of high TNF-α serum levels shortly after trauma.