About: CCR5 Signaling Suppresses Inflammation and Reduces Adverse Remodeling of the Infarcted Heart, Mediating Recruitment of Regulatory T Cells

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About: CCR5 Signaling Suppresses Inflammation and Reduces Adverse Remodeling of the Infarcted Heart, Mediating Recruitment of Regulatory T Cells Goto Sponge NotDistinct Permalink

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	CCR5 Signaling Suppresses Inflammation and Reduces Adverse Remodeling of the Infarcted Heart, Mediating Recruitment of Regulatory T Cells
Creator	Bujak, Marcin Dobaczewski, Marcin Gonzalez-Quesada, Carlos Xia, Ying Frangogiannis, Nikolaos
Source	Elsevier; Medline; PMC
abstract	Myocardial infarction triggers an inflammatory reaction that is involved in cardiac remodeling. Cardiac repair is dependent on regulatory mechanisms that suppress inflammation and prevent excessive matrix degradation. Chemokine induction in the infarcted heart mediates recruitment of leukocyte subsets with distinct properties. We demonstrate that signaling through the CC chemokine receptor 5 (CCR5) prevents uncontrolled postinfarction inflammation and protects from adverse remodeling by recruiting suppressive mononuclear cells. CCR5 and its ligands macrophage inflammatory protein (MIP)−1α and MIP-1β were markedly induced in the infarcted mouse myocardium. In addition, almost 40% of the mononuclear cells infiltrating the infarct expressed CCR5. CCR5(−/−) mice exhibited marked upregulation of proinflammatory cytokine and chemokine expression in the infarct. In wild-type infarcts CCR5(+) mononuclear cells had anti-inflammatory properties, expressing higher levels of IL-10 than CCR5(−) cells. In contrast, mononuclear cells isolated from CCR5(−/−) infarcts had reduced IL-10 expression. Moreover, enhanced inflammation in the absence of CCR5 was associated with impaired recruitment of CD4(+)/foxp3(+) regulatory T cells (Tregs). The CCR5(+) Treg subset exhibited increased IL-10 expression, reflecting potent anti-inflammatory activity. Accentuated inflammation in CCR5(−/−) infarcts was associated with increased matrix metalloproteinase (MMP) expression, reduced TIMP levels, and enhanced MMP-2 and MMP-9 activity, resulting in worse cardiac dilation. These results suggest that CCR5-mediated Treg recruitment may restrain postinfarction inflammation, preventing excessive matrix degradation and attenuating adverse remodeling.
has issue date	2010-05-01(xsd:dateTime)
bibo:doi	10.2353/ajpath.2010.090759
bibo:pmid	20382703
has license	hybrid-oa
sha1sum (hex)	16d2130aa50aa20e39d9302cf7717fb480d7c3da
schema:url	https://doi.org/10.2353/ajpath.2010.090759
resource representing a document's title	CCR5 Signaling Suppresses Inflammation and Reduces Adverse Remodeling of the Infarcted Heart, Mediating Recruitment of Regulatory T Cells
has PubMed Central identifier	PMC2861083
has PubMed identifier	20382703
schema:publication	The American Journal of Pathology
resource representing a document's body	covid:16d2130aa50aa20e39d9302cf7717fb480d7c3da#body_text
is schema:about of	named entity 'SUPPRESSES' named entity 'MOUSE' named entity 'EXPRESSION' named entity 'INCREASED' named entity 'CHEMOKINE' named entity 'PREVENTS' named entity 'INDUCED' named entity 'REMODELING' named entity 'INVOLVED' named entity 'REDUCED' named entity 'PROPERTIES' named entity 'MYOCARDIAL INFARCTION' named entity 'ACCENTUATED' named entity 'INFARCTS' named entity 'LEUKOCYTE' named entity 'CELLS' named entity 'REGULATORY T CELLS' named entity 'DILATION' named entity 'INDUCTION' named entity 'CC CHEMOKINE RECEPTOR 5' named entity 'IMPAIRED' named entity 'MYOCARDIUM' named entity 'SUPPRESSIVE' named entity 'CARDIAC REPAIR' named entity 'SUBSET' named entity 'MATRIX DEGRADATION' named entity 'INFLAMMATION' named entity 'RECRUITMENT' named entity 'UPREGULATION' named entity 'ENHANCED' named entity 'MEDIATING' named entity 'CARDIAC REMODELING' named entity 'UNCONTROLLED' named entity 'REFLECTING' named entity 'HIGHER' named entity 'PREVENT' named entity 'LEVELS' named entity 'REGULATORY T CELLS' named entity 'SIGNALING' named entity 'INFARCTED' named entity 'CCR5' named entity 'RECRUITMENT' named entity 'PREVENTING' named entity 'CYTOKINE ' named entity 'ADDITION' named entity 'INFLAMMATION' named entity 'CARDIAC' named entity 'WORSE' named entity 'RESTRAIN' named entity 'ABSENCE OF' named entity 'MICE' named entity 'TIMP' named entity 'RESULTS' named entity 'MMP-2' named entity 'IL-10' named entity 'DEPENDENT' named entity 'MEDIATED' named entity 'HEART' named entity 'ANTI-INFLAMMATORY ACTIVITY' named entity 'MECHANISMS' named entity 'ACTIVITY' named entity 'TRIGGERS' named entity 'INFARCTED' named entity 'MONONUCLEAR CELLS' named entity 'MIP-1' named entity 'TREG' named entity 'RECRUITING' named entity 'MARKEDLY' named entity 'INFILTRATING' named entity 'HEART' named entity 'MATRIX METALLOPROTEINASE' named entity 'POSTINFARCTION' named entity 'REGULATORY' named entity '90%' named entity '40%' named entity 'PROTEIN ' named entity 'SUGGEST'

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