Apolipoprotein B100 autoimmunity and atherosclerosis - disease mechanisms and therapeutic potential.
Författare
Summary, in English
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.
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.
Avdelning/ar
Publiceringsår
2012
Språk
Engelska
Sidor
422-428
Publikation/Tidskrift/Serie
Current Opinion in Lipidology
Volym
23
Issue
5
Fulltext
- Available as PDF - 812 kB
- Download statistics
Länkar
Dokumenttyp
Artikel i tidskrift
Förlag
Lippincott Williams & Wilkins
Ämne
- Cardiac and Cardiovascular Systems
Status
Published
Forskningsgrupp
- Cardiovascular Research - Immunity and Atherosclerosis
ISBN/ISSN/Övrigt
- ISSN: 1473-6535