Abdominal aortic aneurysm (AAA) is an inflammatory, irreversible dilation of the abdominal aorta, which affects elderly males and is associated with high mortality. In developing AAA macrophages accumulate in the aortic wall either as the pro-inflammatory M1 macrophage releasing cytokines like tumor necrosis factor (TNF), or the tissue repairing M2 macrophage. Besides macrophages, TNF is synthesized in vascular smooth muscle cells and endothelial cells. It exists as a membrane bound (tmTNF) and a soluble form (SolTNF) cleaved by the TNF converting enzyme (TACE). The pro-inflammatory SolTNF acts primarily via activating of TNF receptor (TNFR) 1 and induces apoptosis, while the tissue repairing effect is mediated by tmTNF acting via TNFR2. TNF is elevated in aneurysmal tissue and inhibition of TNF limits AAA expansion in experimental models. However, the cellular source of the elevated TNF levels measured in AAA and its contribution to AAA progression is not fully understood. We hypothesize that a major source of TNF in the aneurysm wall is macrophages and that mice with conditional knockout of TNF in cells of myeloid origin will have smaller AAA compared to controls due to diminished inflammation. Nine weeks old male mice, either lacking tnf in myeloid cells (LysMcrexTNFfl/fl) or their floxed littermate controls (TNFfl/fl) were anaesthetized i.p. with a mixture of ketamine (100 mg/kg) and xylazine (10 mg/kg). AAA was induced by intraluminal elastase infusion for 5 min in the infrarenal region. AAA was allowed to develop within a period of 14 days. AAA size was based on a difference in outer diameter of the abdominal aorta at baseline and day 14 after elastase infusion. Quantitative RT-PCR (qPCR) was performed on RNA isolated from the abdominal aorta 14 days after elastase treatment. Both TNFfl/fl and LysMcrexTNFfl/fl developed AAA, defined by a 50 % increase in aortic diameter, but no difference was found between genotypes (98.3±19.5%, n=8 vs. 121.0±27.3%, n=8, p=0.51). In the aneurysmal tissue no differences between LysMcrexTNFfl/fl and TNFfl/fl in relative TNF mRNA levels (7.60±2.78, n=8 vs. 6.20±1.75, n=8, p=0.68), or TACE mRNA levels (2.01±0.20, n=8 vs. 1.69±0.23, n=8, p=0.32) was observed. Also, no difference between genotypes were detected in the level of the macrophage marker F4/80 (1.18±0.17, n=8 vs. 0.79±0.20, n=8, p=0.16) nor in the M2 macrophage marker CD206 (0.19±0.03, n=8 vs. 0.20±0.030, n=8, p=0.75) or the levels of TNFR1 (5.49±0.80, n=7 vs. 4.93±0.79, n=8, p=0.63), or TNFR2 (8.11±1.03, n=7 vs. 6.94±1.38, n=8, p=0.52). In conclusion, conditional knock out of TNF in myeloid cells does not have an impact on AAA size suggesting that myeloid-derived cells are not the major contributors of aneurysmal TNF at mRNA levels.