Abstract
Historically, the role of adaptive immunity has not been considered to play a major role in the wound healing response to myocardial infarction (MI), due to the low number of these cells within the infarct region. While recent studies have linked elevated CD8+ T‐cell counts (>1065 cells/mm3) with a 2‐fold decrease in post‐MI survival in humans, the exact mechanisms by which CD8+ T‐cells impair cardiac wound healing post‐MI are not thoroughly understood. We hypothesized that CD8+ T‐cells regulate the inflammatory response leading to decreased survival and cardiac function post‐MI. We performed permanent occlusion of the left anterior descending coronary artery on C57BL/6J wild‐type mice (WT; 4.5±0.1 months of age; n=6 males and females) and CD8atm1Mak mice (Null; 4.1±0.2 months of age; n=6 males and females) that are deficient in functional cytotoxic T‐cells. Null had improved day 7 survival (75%) compared to WT (43%; p<0.0001). Interestingly, 100% of Null who died did so due to cardiac rupture of the left ventricle (rupture/total deaths; 2/2) whereas only 38% of WT (3/8; p<0.0001) died of cardiac rupture. In addition, Null died during the early post‐MI phase (at days 1–2). Post‐MI mortality in WT does not usually occur until after day 3, suggesting CD8+ T‐cells may be protective during the early post‐MI phase by limiting immediate remodeling. Echocardiography measured at day 7 post‐MI showed improved cardiac physiology, as indicated by fractional shortening in Null (11±3%) compared to WT (4±1%; p<0.05) implicating CD8+ T‐cells as a negative regulator of wound healing during the later phase post‐MI. In conclusion, our data suggests CD8+ T‐cells play a biphasic role during post‐MI cardiac remodeling by being protective early and detrimental later.Support or Funding InformationThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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