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. 2020 Dec 10;143(8):821–836. doi: 10.1161/CIRCULATIONAHA.120.044581

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© 2020 The Authors.

Circulation is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 7. — Accumulation of cytotoxic CD8⁺ T cells is reduced in both scarred and remote myocardium in Clec9a^−/− mice. Type 1 myocardial infarction was induced in C57BL/6J (WT) and Clec9a^−/− C57BL/6J (KO) mice by permanent ligation of the left anterior descending artery. Hearts were collected 4 weeks after infarction and processed for histology and flow cytometry. A, Example micrographs showing Picrosirius red– and H&E-stained type 1 myocardial infarction heart sections above occlusion, approximately at the ligation point, and below the ligation point. B, Flow cytometry on single cell preparations of isolated scar and remote left ventricular tissue of the heart for quantification of CD3⁺, CD4⁺, and CD8⁺ cells/mg tissue. C, Immunohistochemistry staining for and quantifying numbers of CD8⁺ cells per mm² scar and remote tissue section, respectively. Symbols represent individual mice. Error bars show mean±SEM; *P<0.05; **P<0.001 (1-tailed Student t test with Welch correction). H&E indicates hematoxylin and eosin; KO, knockout; and WT wild type.