• Justine L Newman and James R Stone.
• Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
• Cardiovasc. Pathol. 2019 Nov 1; 43: 107148.

BackgroundImmune checkpoint inhibition (ICI) has emerged as a promising new approach to treat malignancy. Such therapies can result in autoimmune-related complications such as myocarditis and hepatitis. The impact of ICI on sites of preexisting chronic inflammation has been less clear. Atherosclerosis is a chronic vascular disease with a significant inflammatory component.MethodsTo determine the effect of ICI on the inflammatory infiltrate in coronary artery atherosclerotic plaques, 11 patients who had recently been treated with ICI and subsequently underwent autopsy were matched with 11 cancer patients who had not received ICI treatment. The amount of CD3+ T-lymphocytes, CD8+ cytotoxic T-lymphocytes, and CD68+ macrophages and the ratios of the various cell types in the coronary artery atherosclerotic plaques were compared.ResultsThere was no significant difference in the absolute numbers of CD3+, CD8+, or CD68+ cells in the atherosclerotic plaques. In the plaques of the ICI-treated patients, there was a significant increase in the ratio of CD3+ cells to CD68+ cells (CD3/CD68) (P=.002) and a trend towards an increased CD8/CD68 ratio. The increased CD3/CD68 ratio in the ICI-treated patients resulted in 6 of the 11 patients having lymphocyte-predominate inflammation in contrast to the macrophage-predominate inflammation typically found in atherosclerotic plaques.ConclusionsThese findings indicate that ICI alters the inflammatory composition of human atherosclerotic plaque and, thus, may influence plaque progression and/or clinical coronary events.SummaryIn cancer patients, treatment with immune checkpoint inhibition is associated with an altered inflammatory cell composition in coronary artery atherosclerotic plaques with an increased ratio of CD3+ T cells to CD68+ macrophages. Thus, immune checkpoint inhibition may influence plaque progression and/or clinical coronary events.Copyright © 2019 Elsevier Inc. All rights reserved.

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