TY - JOUR
T1 - Preventing autoimmune and infection triggered atherosclerosis for an enduring healthful lifestyle
AU - Matsuura, Eiji
AU - Kobayashi, Kazuko
AU - Lopez, Luis R.
N1 - Funding Information:
The study was supported in part by a research grant-in-aid for scientific research from the Japanese Ministry of Education, Culture, Sports, Science, and Technology.
PY - 2008/1
Y1 - 2008/1
N2 - Atherosclerosis is a chronic inflammatory disease of the arteries associated with various risk factors that promote lipid abnormalities (i.e., dyslipidemia), development and progression of atherosclerotic lesions, plaque rupture, and vascular thrombosis. Experimental evidence from biochemical and clinical studies support the idea that arterial thrombosis is an autoimmune process resulting from 'autoantibody'-mediated pro-atherogenic mechanisms now seen in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). In addition, it has been shown that persistent infections of Clamydia pneumoniae (C. pneumoniae), Porphyromonas gingivalis (P. gingivalis), and Helicobacter pylori (H. pylori) cause immune responses (infectious immunity) in their hosts that promote atherogenesis. In this article, we review recent progress in our understanding of immune- and infection-mediated atherosclerosis.
AB - Atherosclerosis is a chronic inflammatory disease of the arteries associated with various risk factors that promote lipid abnormalities (i.e., dyslipidemia), development and progression of atherosclerotic lesions, plaque rupture, and vascular thrombosis. Experimental evidence from biochemical and clinical studies support the idea that arterial thrombosis is an autoimmune process resulting from 'autoantibody'-mediated pro-atherogenic mechanisms now seen in systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). In addition, it has been shown that persistent infections of Clamydia pneumoniae (C. pneumoniae), Porphyromonas gingivalis (P. gingivalis), and Helicobacter pylori (H. pylori) cause immune responses (infectious immunity) in their hosts that promote atherogenesis. In this article, we review recent progress in our understanding of immune- and infection-mediated atherosclerosis.
KW - Antiphospholipid syndrome (APS)
KW - Atherosclerosis
KW - Infection
KW - Oxidized LDL (oxLDL)
KW - β2-glycoprotein I (β2GPI)
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U2 - 10.1016/j.autrev.2007.11.008
DO - 10.1016/j.autrev.2007.11.008
M3 - Review article
C2 - 18190881
AN - SCOPUS:37648998736
SN - 1568-9972
VL - 7
SP - 214
EP - 222
JO - Autoimmunity Reviews
JF - Autoimmunity Reviews
IS - 3
ER -