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Conventional Dendritic Cells Impair Recovery after Myocardial Infarction

Title
Conventional Dendritic Cells Impair Recovery after Myocardial Infarction
Author
최재훈
Keywords
TRANSCRIPTION FACTOR ZDC; REGULATORY T-CELLS; STEADY-STATE; IN-VIVO; IMMUNE LINEAGES; TREATED MICE; FLT3 LIGAND; MACROPHAGES; MONOCYTES; INFLAMMATION
Issue Date
2018-09
Publisher
AMER ASSOC IMMUNOLOGISTS
Citation
JOURNAL OF IMMUNOLOGY, v. 201, no. 6, page. 1784-1798
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.
URI
https://www.jimmunol.org/content/201/6/1784https://repository.hanyang.ac.kr/handle/20.500.11754/119999
ISSN
0022-1767; 1550-6606
DOI
10.4049/jimmunol.1800322
Appears in Collections:
COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > Articles
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