Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
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The influence of innate and adaptive immune responses on atherosclerosisT cells in atherosclerosisThe Role of TLR2, TLR4, and TLR9 in the Pathogenesis of AtherosclerosisDysregulated CD4+ T cells from SLE-susceptible mice are sufficient to accelerate atherosclerosis in LDLr-/- mice.Batf3-dependent CD8α+ Dendritic Cells Aggravates Atherosclerosis via Th1 Cell Induction and Enhanced CCL5 Expression in Plaque Macrophages.MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases.Disruption of mammalian target of rapamycin complex 1 in macrophages decreases chemokine gene expression and atherosclerosis.Mechanisms that regulate macrophage burden in atherosclerosis.Immune regulation by oral tolerance induces alternate activation of macrophages and reduces markers of plaque destabilization in Apobtm2Sgy/Ldlrtm1Her/J miceInterleukin-3/granulocyte macrophage colony-stimulating factor receptor promotes stem cell expansion, monocytosis, and atheroma macrophage burden in mice with hematopoietic ApoE deficiencySessile alveolar macrophages communicate with alveolar epithelium to modulate immunity.Identification of a non-growth factor role for GM-CSF in advanced atherosclerosis: promotion of macrophage apoptosis and plaque necrosis through IL-23 signaling.Programmed cell death-1 deficiency exacerbates T cell activation and atherogenesis despite expansion of regulatory T cells in atherosclerosis-prone mice.Modulation of recombinant antigenic constructs containing multi-epitopes towards effective reduction of atherosclerotic lesion in B6;129S-Ldlr(tm1Her)Apob(tm2Sgy)/J miceMHC Class II-restricted antigen presentation by plasmacytoid dendritic cells drives proatherogenic T cell immunitySuppression of Adaptive Immune Cell Activation Does Not Alter Innate Immune Adipose Inflammation or Insulin Resistance in ObesityTLR2 and TLR9 contribute to alcohol-mediated liver injury through induction of CXCL1 and neutrophil infiltration.Beyond vascular inflammation--recent advances in understanding atherosclerosis.The immune system in Duchenne muscular dystrophy: Friend or foe.Recipient Myd88 Deficiency Promotes Spontaneous Resolution of Kidney Allograft RejectionTAK1 regulates Paneth cell integrity partly through blocking necroptosis.The role of the vascular dendritic cell network in atherosclerosis.Toll-like receptors in atherosclerosis2015 Russell Ross Memorial Lecture in Vascular Biology: Protective Autoimmunity in AtherosclerosisImmune effector mechanisms implicated in atherosclerosis: from mice to humans.Why targeting HDL should work as a therapeutic tool, but has not.Molecular sources of residual cardiovascular risk, clinical signals, and innovative solutions: relationship with subclinical disease, undertreatment, and poor adherence: implications of new evidence upon optimizing cardiovascular patient outcomes.Inflammation and plaque vulnerability.Molecular Mechanisms That Underlie the Dynamic Adaptation of Innate Monocyte Memory to Varying Stimulant Strength of TLR LigandsLipid-Free Apolipoprotein A-I Reduces Progression of Atherosclerosis by Mobilizing Microdomain Cholesterol and Attenuating the Number of CD131 Expressing Cells: Monitoring Cholesterol Homeostasis Using the Cellular Ester to Total Cholesterol Ratio.Microdomains, Inflammation, and Atherosclerosis.Dendritic cells in atherosclerosis.Macrophage mitochondrial oxidative stress promotes atherosclerosis and nuclear factor-κB-mediated inflammation in macrophages.Myeloid cells in atherosclerosis: a delicate balance of anti-inflammatory and proinflammatory mechanisms.The dynamic lives of macrophage and dendritic cell subsets in atherosclerosis.Treating atherosclerosis with regulatory T cells.Atheroprotective immunity and cardiovascular disease: therapeutic opportunities and challenges.Readapting the adaptive immune response - therapeutic strategies for atherosclerosis.Quercetin protects against atherosclerosis by inhibiting dendritic cell activation.Toll-like receptors: promising therapeutic targets for inflammatory diseases.
P2860
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P2860
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年学术文章
@wuu
2012年学术文章
@zh-cn
2012年学术文章
@zh-hans
2012年学术文章
@zh-my
2012年学术文章
@zh-sg
2012年學術文章
@yue
2012年學術文章
@zh
2012年學術文章
@zh-hant
name
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
@ast
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
@en
type
label
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
@ast
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
@en
prefLabel
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
@ast
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
@en
P2093
P2860
P356
P1476
Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs.
@en
P2093
Edward Thorp
Goran K Hansson
Manikandan Subramanian
P2860
P304
P356
10.1172/JCI64617
P407
P577
2012-12-21T00:00:00Z