Innate and acquired immunity in atherogenesis
By C. Binder, Mi-Kyung Chang, P. Shaw, Yury I. Miller, K. Hartvigsen, A. Dewan, J. Witztum. Nature Medicine, 2002
706 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/da16445ef4583d215d69c20f8dd071a8a73c0025
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Citations in the corpus
- Antiinflammatory Properties of HDL (2004, background): “Thus, antibodies to the oxidized phospholipids found in MM-LDL appear to be “preloaded” in the innate immune system [29].”
- Reduced atherosclerosis in MyD88-null mice links elevated serum cholesterol levels to activation of innate immunity signaling pathways (2004, background): “The search for proinflammatory signaling cascades activated by endogenous lipoproteins has recently focused on the TLRs, a group of pattern-recognition receptors that activate host defenses in response to microbial-derived ligand”
- Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases. (2018, background): “The recruitment of LDL cholesterol into the arterial wall also leads to activation of the NLRP3 inflammasome, since excess cholesterol is partially deposited as cholesterol crystals [157-158], which are fully internalized by human macrophages by phagocytosis and promote IL-1β and IL-18 generation [1”
- Cytokines in atherosclerosis: pathogenic and regulatory pathways. (2006, background): “Several excellent reviews have been published on the theme of atherosclerosis and inflammation since the founding Ross review (52, 235, 265, 395, 417, 578).”
- Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury (2008, background): “including OxPLs, have been implicated as pathogen-associated molecular patterns that are detected by several conserved pattern-recognition receptors (Binder et al., 2002; Miller et al., 2003b).”
- NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases (2015, neutral): “…. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304”
- Oxidative metabolism and PGC-1beta attenuate macrophage-mediated inflammation. (2006, background): “Development and progression of atherosclerotic plaques is dictated by a balance between proand anti-inflammatory factors (Binder et al., 2002;Hansson, 2005).”
- Pneumococcal vaccination decreases atherosclerotic lesion formation: molecular mimicry between Streptococcus pneumoniae and oxidized LDL (2003, background): “Moreover, growing evidence suggests that both adaptive and innate immune mechanisms can modulate the progression of atherosclerosi”