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Apolipoprotein B100 autoimmunity and atherosclerosis - disease mechanisms and therapeutic potential.

Nilsson, Jan LU ; Björkbacka, Harry LU and Nordin Fredrikson, Gunilla LU (2012) In Current Opinion in Lipidology 23(5). p.422-428
Abstract
PURPOSE OF REVIEW:

Adaptive immune responses have been shown to play an important role in the atherosclerotic disease process and both pathogenic and protective immunity has been identified. Apolipoprotein (apo) B100 appears to be a key antigen and novel therapies modulating immune responses against apo B100 have shown promising results in experimental models. This review will discuss recent developments in the mechanistic understanding of apo B100 autoimmunity and approaches taken to use this knowledge for development of novel therapies.



RECENT FINDINGS:

It has recently been shown that not only apo B100 modified by oxidation but also nonmodified apo B100 is targeted by autoimmune responses. This... (More)
PURPOSE OF REVIEW:

Adaptive immune responses have been shown to play an important role in the atherosclerotic disease process and both pathogenic and protective immunity has been identified. Apolipoprotein (apo) B100 appears to be a key antigen and novel therapies modulating immune responses against apo B100 have shown promising results in experimental models. This review will discuss recent developments in the mechanistic understanding of apo B100 autoimmunity and approaches taken to use this knowledge for development of novel therapies.



RECENT FINDINGS:

It has recently been shown that not only apo B100 modified by oxidation but also nonmodified apo B100 is targeted by autoimmune responses. This implies that a corresponding set of regulatory T cells with the same antigen specificity must exist and that these cells under normal circumstances are able to prevent autoimmunity against LDL. Recent studies also suggest that the atheroprotective effect of apo B100 peptide immunization acts by re-enforcing the activity of such cells.



SUMMARY:

These novel findings suggest that aggravation of plaque inflammation may occur as a result of a local loss of tolerance against LDL in the plaque due to insufficient activity of regulatory T cells. Restoration of lost tolerance represents an interesting novel approach for treatment of cardiovascular disease. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Current Opinion in Lipidology
volume
23
issue
5
pages
422 - 428
publisher
Lippincott Williams & Wilkins
external identifiers
  • wos:000308798100003
  • pmid:22814703
  • scopus:84866307958
ISSN
1473-6535
DOI
10.1097/MOL.0b013e328356ec7c
language
English
LU publication?
yes
id
c16e5f99-779e-4940-ab66-7b96f4b6c3c6 (old id 2966859)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/22814703?dopt=Abstract
date added to LUP
2012-08-09 20:15:20
date last changed
2017-11-12 03:09:42
@article{c16e5f99-779e-4940-ab66-7b96f4b6c3c6,
  abstract     = {PURPOSE OF REVIEW: <br/><br>
Adaptive immune responses have been shown to play an important role in the atherosclerotic disease process and both pathogenic and protective immunity has been identified. Apolipoprotein (apo) B100 appears to be a key antigen and novel therapies modulating immune responses against apo B100 have shown promising results in experimental models. This review will discuss recent developments in the mechanistic understanding of apo B100 autoimmunity and approaches taken to use this knowledge for development of novel therapies. <br/><br>
<br/><br>
RECENT FINDINGS: <br/><br>
It has recently been shown that not only apo B100 modified by oxidation but also nonmodified apo B100 is targeted by autoimmune responses. This implies that a corresponding set of regulatory T cells with the same antigen specificity must exist and that these cells under normal circumstances are able to prevent autoimmunity against LDL. Recent studies also suggest that the atheroprotective effect of apo B100 peptide immunization acts by re-enforcing the activity of such cells. <br/><br>
<br/><br>
SUMMARY: <br/><br>
These novel findings suggest that aggravation of plaque inflammation may occur as a result of a local loss of tolerance against LDL in the plaque due to insufficient activity of regulatory T cells. Restoration of lost tolerance represents an interesting novel approach for treatment of cardiovascular disease.},
  author       = {Nilsson, Jan and Björkbacka, Harry and Nordin Fredrikson, Gunilla},
  issn         = {1473-6535},
  language     = {eng},
  number       = {5},
  pages        = {422--428},
  publisher    = {Lippincott Williams & Wilkins},
  series       = {Current Opinion in Lipidology},
  title        = {Apolipoprotein B100 autoimmunity and atherosclerosis - disease mechanisms and therapeutic potential.},
  url          = {http://dx.doi.org/10.1097/MOL.0b013e328356ec7c},
  volume       = {23},
  year         = {2012},
}