Lack of Toll-like receptor 4 or myeloid differentiation factor 88 reduces atherosclerosis and alters plaque phenotype in mice deficient in apolipoprotein E.

By K. Michelsen, M. Wong, P. Shah, Wenxuan Zhang, J. Yano, T. M. Doherty, Shizuo Akira, T. Rajavashisth, M. Arditi. Proceedings of the National Academy of Sciences of the United States of America, 2004

1,084 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/3e0f5bd7d535c08f8a38722bdfaaece1b3f2f921

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In Immunology

1. Shizuo Akira
2. M. Karin
3. Peter Libby
4. Luke A. O'Neill
5. G. Hansson
6. T. Lawrence
7. R. Medzhitov
8. G. Núñez

Citations in the corpus

• CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer (2009, background): “We therefore tested whether fibrillar β-amyloid peptide (1-42) (Aβ1-42) could activate TLR4-TLR6 signaling via CD36.”
• NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases (2015, background): “Myeloid differentiation primary response protein 88 and the kinase activity of IL-1β receptor-associated kinase-4 have also been implicated in the NLRP3 activation mechanism [162,163].”
• Innate immunity gone awry: linking microbial infections to chronic inflammation and cancer. (2006, background): “Consistent with this notion, TLR4-deficient mice are resistant to development of diet-induced atherosclerosis, a chronic inflammatory disease of the vasculature (Michelsen et al., 2004).”
• Sterile inflammation: sensing and reacting to damage (2010, background): “Deficiency in either TLR2 or TLR4 signalling also reduced atherosclerotic disease in mouse model”
• Cholesterol Crystals Activate the NLRP3 Inflammasome in Human Macrophages: A Novel Link between Cholesterol Metabolism and Inflammation (2010, background): “Several lines of evidence indicate that TLR signaling is operative in atherosclerotic arterial intima, and may contribute to disease pathogenesis [43,44].”
• Identification of Oxidative Stress and Toll-like Receptor 4 Signaling as a Key Pathway of Acute Lung Injury (2008, background): “…and Acute Lung Injury via TLR4 Minimally modified low-density lipoprotein (LDL) has been previously shown to mediate macrophage activation (Miller et al., 2003a, 2005) and to modulate the severity of atherosclerosis and inflammatory responses via TLR4 (Miller et al., 2003a; Michelsen et al., 2004).”
• The immune system in atherosclerosis (2011, background): “Knockout studies of hypercholesterolemic mice have demonstrated a major proatherosclerotic role for MyD88, a key adaptor protein in the signaling cascades of most TLR”
• Cytokines in atherosclerosis: pathogenic and regulatory pathways. (2006, result): “Two lines of evidence support this hypothesis: 1) oxLDL enhances TLR4 expression in macrophages (760), and 2) TLR4 or its intracellular adaptor protein, MyD88, reduces atherosclerosis in uninfected apoE-deficient mice, concomitant with a marked reduction in macrophage infiltration and MCP-1 expressi”
• Negative regulation of Toll-like receptor-mediated immune responses (2005, background): “fcgi?db=gene&cmd=Retrieve&dopt=Graphics&&list_uids=4615">MyD88 , a TLR-signalling adaptor protein, are less prone to atherosclerosi”