Adoptive transfer of T cells from aged mice exhibited increased cardiotropism compared with young donors, indicating T cells contribute to age-related myocardial inflammation and functional decline.
Myocardial aging
Adoptive cell transfer of T cells from aged animals vs T cells from young donors or irrelevant sites
Cardiotropism and cardiac functionality
T cells in the heart-draining lymph nodes. A comprehensive characterization of different aged immune-deficient mouse strains revealed that T cells significantly contribute to age-related myocardial inflammation and functional decline. Upon adoptive cell transfer, the T cells isolated from the mediastinal lymph node (med-LN) of aged animals exhibited increased cardiotropism, compared with cells purified from young donors or from other irrelevant sites. Nevertheless, these cells caused rather mild effects on cardiac functionality, indicating that myocardial aging might stem from a combination of intrinsic and extrinsic (immunological) factors. Taken together, the data herein presented indicate that heart-directed immune responses may spontaneously arise in the elderly, even in the absence of a clear tissue damage or concomitant infection. These observations might shed new light on the emerging role of T cells in myocardial diseases, which primarily affect the elderly population.
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Gustavo C. Ramos
Universitätsklinikum Würzburg
Anne van den Berg
Erasmus MC
Vânia Silva
Universidade Estadual de Maringá
Proceedings of the National Academy of Sciences
University of Würzburg
Instituto Gulbenkian de Ciência
University Hospital in Halle
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Ramos et al. (Thu,) conducted a other in Myocardial aging. Adoptive cell transfer of T cells from aged animals vs. T cells from young donors or irrelevant sites was evaluated on Cardiotropism and cardiac functionality. Adoptive transfer of T cells from aged mice exhibited increased cardiotropism compared with young donors, indicating T cells contribute to age-related myocardial inflammation and functional decline.
synapsesocial.com/papers/6a0ba9ae4f6759c6fca255fc — DOI: https://doi.org/10.1073/pnas.1621047114