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Conventional Dendritic Cells Impair Recovery after Myocardial Infarction

Title
Conventional Dendritic Cells Impair Recovery after Myocardial Infarction
Authors
Lee, Jun SeongJeong, Se-JinKim, SinaiChalifour, LorraineYun, Tae JinMiah, Mohammad AlamLi, BinMajdoubi, AbdelilahSabourin, AntoineKeler, TiborGuimond, Jean V.Haddad, ElieChoi, Eui-YoungEpelman, SlavaChoi, Jae-HoonThibodeau, JacquesOh, Goo TaegCheong, Cheolho
Ewha Authors
오구택
SCOPUS Author ID
오구택scopus
Issue Date
2018
Journal Title
JOURNAL OF IMMUNOLOGY
ISSN
0022-1767JCR Link

1550-6606JCR Link
Citation
JOURNAL OF IMMUNOLOGY vol. 201, no. 6, pp. 1784 - 1798
Publisher
AMER ASSOC IMMUNOLOGISTS
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Ischemic myocardial injury results in sterile cardiac inflammation that leads to tissue repair, two processes controlled by mono-nuclear 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-1 beta and IFN-gamma were reduced. Collectively, our results demonstrate the unequivocal pathological role of cDCs following MI.
DOI
10.4049/jimmunol.1800322
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자연과학대학 > 생명과학전공 > Journal papers
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