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AIMS Here we investigate whether chronic hyperglycaemia in T1D is associated with a pro-inflammatory immune signature and with arterial wall inflammation, driving the development of atherosclerosis. METHODS AND RESULTS We recruited patients with T1D (n = 41), and healthy age-, sex- and BMI-matched controls (n = 20). Arterial wall inflammation and hematopoietic activity was measured with 2'-deoxy-2'-(18F)-fluoro-D-glucose (18F-FDG) positron emission tomography/computed tomography (PET/CT). In addition, flow cytometry of circulating leukocytes was performed as well as targeted proteomics to measure circulating inflammatory markers. 18F-FDG uptake in the wall of the abdominal aorta, carotid arteries and iliac arteries was higher in T1D compared to the healthy controls. Also, 18F-FDG uptake in the bone marrow and spleen was higher in T1D patients. CCR2 and CD36 expression on circulating monocytes was higher in T1D patients, as well as several circulating inflammatory proteins. In addition, several circulating inflammatory markers (OPG, TGF-alpha, CX3CL1 and CSF-1) displayed a positive correlation with FDG uptake. Within T1D, no differences were found between people with a high and low HbA1c. CONCLUSION Our findings strengthen the concept that chronic hyperglycaemia in T1D induces inflammatory changes that fuel arterial wall inflammation leading to atherosclerosis. The degree of hyperglycaemia appears to play a minor role in driving this inflammatory response in patients with T1D. TRANSLATIONAL PERSPECTIVE Arterial wall inflammation is associated with increased levels of several circulating inflammatory markers suggesting that these proteins are directly involved in driving this process yet may also serve as future biomarkers to identify patients with T1D at risk for the development of CVD. And could potentially be future treatment targets in reducing the risk of CVD in people with T1D.