Gene expression profile of myosin-specific CD4+ T-cells activated after myocardial infarction
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PROVIDER: PRJNA479420 | ENA |
REPOSITORIES: ENA
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Project description:Pathological expansion of self-reactive T cells is a hallmark of autoimmune diseases. Notwith-standing, T cell autoreactivity can also benefit self-maintenance and foster tissue repair. Herein, we investigated whether heart-specific T cells exert salutary or detrimental effects in the context of the post myocardial infarction (MI) healing process in mice, and whether the findings can be translated to humans. Transferred cardiac-myosin-specific CD4+ T cells (TCR-M) selectively accumulate in the myocardium and mediastinal lymph nodes (med-LNs) of infarcted mice. TCR-M cells activated in the MI-context acquire a Foxp3+ regulatory phenotype, exhibit a distinct gene expression profile enriched with growth factors, and promote cardioprotection. Massive parallel sequencing of T cell receptors revealed that CD4+ T cells infiltrating the infarcted myo-cardium display a unique repertoire signature with skewed diversity and dominated by a limited set of expanded clones - hallmarks of antigen-specific responses. CD4+ Foxp3+ cells were also detected in myocardial biopsies obtained from patients who suffered MI, especially in associa-tion with the granulation tissue (i.e., healing phase). Noninvasive positron emission tomogra-phy/computed tomography (PET/CT) imaging using a CXCR4 radioligand revealed that MI pa-tients display enlarged med-LNs with increased T cellularity. Alterations in the med-LN corre-lated with infarct size and cardiac function. Taken together, these results provide strong evidence that the MI-context induces protective T cell autoimmunity in mice, and confirm the existence of an analogous physiological heart/med-LN/T cell axis in MI patients, which offers translational potential.
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