Autoimmune mechanisms of atherosclerosis

Kaushik Mandal, M. Jahangiri, Q. Xu

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Accumulating evidence supports an autoimmune mechanism as one of the prime pathogenic processes involved in the development of atherosclerosis. So far, three proteins, including heat shock proteins (HSPs), oxidized low-density lipoprotein (oxLDL), and ß2 glycoprotein1 (ß2GP1) have been recognized as autoantigens. It has been demonstrated that risk factors for atherosclerosis, such as hypercholesterolemia, hypertension, infections, and oxidative stress, evoke increased expression of HSPs in cells of atherosclerotic lesions. Autoantibody levels against HSPs are significantly increased in patients with atherosclerosis and T lymphocytes specifically responding to these autoantigens have been demonstrated within atherosclerotic plaques. Subcutaneous immunization of animals with HSP65 induced atheroma formation in the arterial wall. Furthermore, circulating immunoglobulin (Ig) G and IgM oxidized low-density lipoprotein (oxLDL) antibodies are present in the plasma of animals and humans and form immune complexes with oxLDL in atherosclerotic lesions. These antibodies closely correlate with the progression and regression of atherosclerosis in murine models. Interestingly, recent reports demonstrated that pneumococcal vaccination to LDL receptor-deficient mice results in elevation of anti-oxLDL IgM Ab EO6, which is inversely correlated with the development of atherosclerosis. Finally, it has been observed that autoantigen ß2GP1 localizes in the atheroma and that autoantibodies to ß2GP1 are correlated with the incidence of atherosclerosis in patients. Hence, these autoimmune reactions to HSPs, oxLDL and ß2GP1 can contribute to the initiation and progression of atherosclerosis.

Original languageEnglish (US)
Title of host publicationHandbook of Experimental Pharmacology
Pages723-743
Number of pages21
Volume170
DOIs
StatePublished - 2005
Externally publishedYes

Publication series

NameHandbook of Experimental Pharmacology
Volume170
ISSN (Print)01712004
ISSN (Electronic)18650325

Fingerprint

Atherosclerosis
Heat-Shock Proteins
Atherosclerotic Plaques
Autoantigens
LDL Lipoproteins
Autoantibodies
Immunoglobulin M
Animals
Immunization
Oxidative stress
T-cells
Antibodies
LDL Receptors
Antigen-Antibody Complex
Immunoglobulin G
oxidized low density lipoprotein
Hypercholesterolemia
Plasmas
Vaccination
Oxidative Stress

Keywords

  • Atherosclerosis
  • Autoimmunity
  • Beta2 glycoprotein1 (ß2GP1)
  • Heat shock protein (HSP)
  • Oxidised LDL (oxLDL)

ASJC Scopus subject areas

  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry

Cite this

Mandal, K., Jahangiri, M., & Xu, Q. (2005). Autoimmune mechanisms of atherosclerosis. In Handbook of Experimental Pharmacology (Vol. 170, pp. 723-743). (Handbook of Experimental Pharmacology; Vol. 170). https://doi.org/10.1007/3-540-27661-0-27

Autoimmune mechanisms of atherosclerosis. / Mandal, Kaushik; Jahangiri, M.; Xu, Q.

Handbook of Experimental Pharmacology. Vol. 170 2005. p. 723-743 (Handbook of Experimental Pharmacology; Vol. 170).

Research output: Chapter in Book/Report/Conference proceedingChapter

Mandal, K, Jahangiri, M & Xu, Q 2005, Autoimmune mechanisms of atherosclerosis. in Handbook of Experimental Pharmacology. vol. 170, Handbook of Experimental Pharmacology, vol. 170, pp. 723-743. https://doi.org/10.1007/3-540-27661-0-27
Mandal K, Jahangiri M, Xu Q. Autoimmune mechanisms of atherosclerosis. In Handbook of Experimental Pharmacology. Vol. 170. 2005. p. 723-743. (Handbook of Experimental Pharmacology). https://doi.org/10.1007/3-540-27661-0-27
Mandal, Kaushik ; Jahangiri, M. ; Xu, Q. / Autoimmune mechanisms of atherosclerosis. Handbook of Experimental Pharmacology. Vol. 170 2005. pp. 723-743 (Handbook of Experimental Pharmacology).
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