Fig 1: TREM2 overexpression improves tissue repair through restricting autoimmunity. (A) Experimental design: TREM2 KO MI mice were injected TREM2 adenovirus (Ad-TREM2) or control vector (Ad-null), followed by flow cytometry (FCM), immunofluorescence staining (IF), Masson staining, magnetic resonance imaging (MRI), and echocardiographic (Ehco) analysis at specified time points. (B) Representative 9.4 T cardiac MRI imagines in Sham / MI mice. Scale bar: 3 mm (left), 0.5 mm (right). (C) Echocardiographic analysis of left ventricular (LV) ejection fraction (EF), (D) LV end-diastolic volume, (E) fractional shortening (FS), (F) LV end-systolic volume (n = 3, 5). (G) Masson staining (Scale bar: 1 mm) and (H) quantification of infarct size, 28d post-MI (n = 4). (I) IF of CD3 / CD8 in the infarct border zone at MI-7d (n = 4, Scale bar: 25 μm). (J) FCM analysis showing the proportions of CD8+ T cells in infarct hearts, MI-7d (n = 7). (K) Flow cytometry analysis of CD8+ T cells in control and ozanimod treatment Ad-TREM2 mice' infarcted hearts at MI-7d (n = 4). (L) ELISA results of CXCL16, infarct areas, MI-7d (n = 6). (M) IF of Lyve1 and Ki67 in the infarct border zone (Scale bar: 25 μm). Quantified (N) percentage of Ki67+ lymphatic endothelial cells (LECs) and (O) LEC area (Lyve1 staining) (n=3). (P) Western blot images and (Q) quantification adjacent of VEGFC in the infarct hearts, MI-7d (n = 3). Data are presented as the mean ± SD. Unpaired student t test. *p < 0.05, **p < 0.01.