PMID- 11209978
OWN - NLM
STAT- MEDLINE
DCOM- 20010405
LR  - 20061115
IS  - 0785-3890 (Print)
IS  - 0785-3890 (Linking)
VI  - 32 Suppl 1
DP  - 2000 Dec
TI  - Antiphospholipid antibodies in arterial thrombosis.
PG  - 27-31
AB  - The high correlation between the IgG isotype of anticardiolipin antibodies (aCLs) 
      and clinical thrombosis was first documented in 1983, and this observation was 
      confirmed in subsequent studies. In addition, the frequency of fetal loss and 
      thrombocytopenia was increased in this group of patients. These findings were 
      termed the antiphospholipid syndrome (APS). This syndrome was mostly seen in 
      patients with systemic lupus erythematosus (SLE), but it soon became clear that 
      also other patients not suffering from defined SLE might exhibit features of APS. 
      aCL in APS patients are detected in immunoassays by using solid phase cardiolipin 
      as a putative antigen. However, antibodies directed against phospholipid-binding 
      plasma or serum proteins, beta2-glycoprotein I (beta2-GPI), in particular, are 
      also detected. Many recent studies have indicated that one of predominant 
      antibodies that has been identified as aCL in APS patients is against beta2-GPI 
      rather than any of the negatively charged phospholipids. The epitopes recognized 
      by anti-beta2-GPI antibodies raised in APS patients are composed of discontinuous 
      amino acid sequences from the IV domain of human beta2-GPI. These epitopes are 
      cryptic when beta2-GPI does not interact with anionic phospholipids. An early 
      event in atherosclerosis is the accumulation of cholesterol-laden foam cells, 
      which originate mainly from monocyte-macrophage cells by their uptake of 
      chemically modified low-density lipoprotein (LDL). We found that beta2-GPI binds 
      directly to oxLDL, and that the complex of oxLDL and beta2-GPI is subsequently 
      recognized by aCL (anti-beta2-GPI) to be taken up by macrophages. While the 
      pathogenesis of this accelerated atherosclerosis is likely to be multifactorial, 
      it is possible that antiphospholipid antibodies, including aCL (anti-beta2-GPI 
      antibodies), may have contributed to the formation of atherosclerotic lesion.
FAU - Koike, T
AU  - Koike T
AD  - Department of Medicine II, Hokkaido University School of Medicine, Sapporo, 
      Japan. tkoike@med.hokudai.ac.jp
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Ann Med
JT  - Annals of medicine
JID - 8906388
RN  - 0 (Antibodies, Antiphospholipid)
RN  - 0 (Epitopes)
RN  - 0 (Glycoproteins)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (beta 2-Glycoprotein I)
SB  - IM
MH  - Antibodies, Antiphospholipid/*immunology
MH  - Antiphospholipid Syndrome/immunology
MH  - Arteriosclerosis/immunology
MH  - Coronary Disease/immunology
MH  - Epitopes/immunology
MH  - Glycoproteins/immunology/physiology
MH  - Humans
MH  - Lipoproteins, LDL/immunology
MH  - Lupus Erythematosus, Systemic/immunology
MH  - Membrane Glycoproteins/immunology/physiology
MH  - Thrombosis/*immunology
MH  - beta 2-Glycoprotein I
RF  - 28
EDAT- 2001/02/24 12:00
MHDA- 2001/04/06 10:01
CRDT- 2001/02/24 12:00
PHST- 2001/02/24 12:00 [pubmed]
PHST- 2001/04/06 10:01 [medline]
PHST- 2001/02/24 12:00 [entrez]
PST - ppublish
SO  - Ann Med. 2000 Dec;32 Suppl 1:27-31.