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Conventional Dendritic Cells Impair Recovery after Myocardial Infarction

 Jun Seong Lee  ;  Se-Jin Jeong  ;  Sinai Kim  ;  Lorraine Chalifour  ;  Tae Jin Yun  ;  Mohammad Alam Miah  ;  Bin Li  ;  Abdelilah Majdoubi  ;  Antoine Sabourin  ;  Tibor Keler  ;  Jean V. Guimond  ;  Elie Haddad  ;  Eui-Young Choi  ;  Slava Epelman  ;  Jae-Hoon Choi  ;  Jacques Thibodeau  ;  Goo Taeg Oh  ;  Cheolho Cheong 
 JOURNAL OF IMMUNOLOGY, Vol.201(6) : 1784-1798, 2018 
Journal Title
Issue Date
Ischemic myocardial injury results in sterile cardiac inflammation that leads to tissue repair, two processes controlled by mononuclear phagocytes. Despite global burden of cardiovascular diseases, we do not understand the functional contribution to pathogenesis of specific cardiac mononuclear phagocyte lineages, in particular dendritic cells. To address this limitation, we used detailed lineage tracing and genetic studies to identify bona fide murine and human CD103+ conventional dendritic cell (cDC)1s, CD11b+ cDC2s, and plasmacytoid DCs (pDCs) in the heart of normal mice and immunocompromised NSG mice reconstituted with human CD34+ cells, respectively. After myocardial infarction (MI), the specific depletion of cDCs, but not pDCs, improved cardiac function and prevented adverse cardiac remodeling. Our results showed that fractional shortening measured after MI was not influenced by the absence of pDCs. Interestingly, however, depletion of cDCs significantly improved reduction in fractional shortening. Moreover, fibrosis and cell areas were reduced in infarcted zones. This correlated with reduced numbers of cardiac macrophages, neutrophils, and T cells, indicating a blunted inflammatory response. Accordingly, mRNA levels of proinflammatory cytokines IL-1β and IFN-γ were reduced. Collectively, our results demonstrate the unequivocal pathological role of cDCs following MI.
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Choi, Eui Young(최의영) ORCID logo https://orcid.org/0000-0003-3732-0190
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