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Conventional Dendritic Cells Impair Recovery after Myocardial Infarction

Jun Seong Lee1,2,3, Se-Jin Jeong4, Sinai Kim4

  • 1Département de Microbiologie, Infectiologie et Immunologie, Université de Montréal, Montreal, Quebec H3T 1J4, Canada.

Journal of Immunology (Baltimore, Md. : 1950)
|August 12, 2018
PubMed

Insights

Conventional dendritic cells (cDCs) worsen heart damage after myocardial infarction (MI). Depleting cDCs improves cardiac function and reduces inflammation, revealing their pathological role in heart repair.

Area of Science:

  • Immunology
  • Cardiology
  • Pathology

Background:

  • Myocardial infarction (MI) triggers sterile cardiac inflammation and tissue repair, processes regulated by mononuclear phagocytes.
  • The specific roles of cardiac mononuclear phagocyte subsets, particularly dendritic cells, in cardiovascular disease pathogenesis remain unclear.

Purpose of the Study:

  • To investigate the functional contribution of specific cardiac dendritic cell (DC) subsets to cardiac injury and repair following myocardial infarction.
  • To identify and characterize murine and human DC populations within the heart.

Main Methods:

  • Utilized lineage tracing and genetic studies to identify CD103+ conventional DC1s (cDC1s), CD11b+ conventional DC2s (cDC2s), and plasmacytoid DCs (pDCs) in murine and humanized mouse hearts.
  • Assessed cardiac function, remodeling, fibrosis, and inflammatory cell infiltration after MI in DC-depleted models.

Main Results:

  • Specific depletion of cDCs, but not pDCs, significantly improved cardiac function and prevented adverse cardiac remodeling post-MI.
  • Reduced infarct zone fibrosis, cell area, and inflammatory cell infiltration (macrophages, neutrophils, T cells) were observed in cDC-depleted hearts.
  • Depletion of cDCs led to decreased expression of pro-inflammatory cytokines IL-1β and IFN-γ.

Conclusions:

  • Conventional dendritic cells play a critical pathological role in the response to myocardial infarction.
  • Targeting cDCs may represent a therapeutic strategy to mitigate cardiac damage and improve outcomes after MI.

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