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Regulation of immune mechanisms in atherosclerosis.
Ann N Y Acad Sci. 2001 Dec; 947:157-65; discussion 165-6.AN

Abstract

Atherosclerosis is accompanied by a local immune response in plaque, but its role in the pathogenesis of the disease is still unclear. Although we might expect that an (auto)immune response would be an aggravating factor, some of its consequences could be protective. Studies of human plaques and of lesion formation in apo E-0 mice show that CD4+ T cells and macrophages form an inflammatory infiltrate. Both cell types are activated and secrete proinflammatory cytokines. CD4+ cells respond immunospecifically to oxidized LDL, suggesting that oxidation induces antigenic epitopes on LDL and converts it to an autoantigen. The pathophysiological consequences of this response are probably mediated largely via cytokine secretion and cell-cell contacts. Th1 cytokines dominate and may promote vascular inflammation; this is enhanced by the increased capacity for activation of NF-kappaB in intimal smooth muscle cells. The net effect of such activity appears to be proatherogenic, as can be deduced by cell transfer into immunodeficient apoE-0 x SCID mice. These data emphasize the importance of inflammation and immune responses in the pathogenesis of atherosclerosis.

Authors+Show Affiliations

Department of Medicine and Center for Molecular Medicine, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden. Goran.Hansson@cmm.ki.se

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

11795263

Citation

Hansson, G K.. "Regulation of Immune Mechanisms in Atherosclerosis." Annals of the New York Academy of Sciences, vol. 947, 2001, pp. 157-65; discussion 165-6.
Hansson GK. Regulation of immune mechanisms in atherosclerosis. Ann N Y Acad Sci. 2001;947:157-65; discussion 165-6.
Hansson, G. K. (2001). Regulation of immune mechanisms in atherosclerosis. Annals of the New York Academy of Sciences, 947, 157-65; discussion 165-6.
Hansson GK. Regulation of Immune Mechanisms in Atherosclerosis. Ann N Y Acad Sci. 2001;947:157-65; discussion 165-6. PubMed PMID: 11795263.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Regulation of immune mechanisms in atherosclerosis. A1 - Hansson,G K, PY - 2002/1/25/pubmed PY - 2002/2/2/medline PY - 2002/1/25/entrez SP - 157-65; discussion 165-6 JF - Annals of the New York Academy of Sciences JO - Ann. N. Y. Acad. Sci. VL - 947 N2 - Atherosclerosis is accompanied by a local immune response in plaque, but its role in the pathogenesis of the disease is still unclear. Although we might expect that an (auto)immune response would be an aggravating factor, some of its consequences could be protective. Studies of human plaques and of lesion formation in apo E-0 mice show that CD4+ T cells and macrophages form an inflammatory infiltrate. Both cell types are activated and secrete proinflammatory cytokines. CD4+ cells respond immunospecifically to oxidized LDL, suggesting that oxidation induces antigenic epitopes on LDL and converts it to an autoantigen. The pathophysiological consequences of this response are probably mediated largely via cytokine secretion and cell-cell contacts. Th1 cytokines dominate and may promote vascular inflammation; this is enhanced by the increased capacity for activation of NF-kappaB in intimal smooth muscle cells. The net effect of such activity appears to be proatherogenic, as can be deduced by cell transfer into immunodeficient apoE-0 x SCID mice. These data emphasize the importance of inflammation and immune responses in the pathogenesis of atherosclerosis. SN - 0077-8923 UR - https://www.unboundmedicine.com/medline/citation/11795263/Regulation_of_immune_mechanisms_in_atherosclerosis_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0077-8923&date=2001&volume=947&spage=157 DB - PRIME DP - Unbound Medicine ER -