PMID- 15546799
OWN - NLM
STAT- MEDLINE
DCOM- 20050419
LR  - 20081121
IS  - 1568-9972 (Print)
IS  - 1568-9972 (Linking)
VI  - 3
IP  - 7-8
DP  - 2004 Nov
TI  - Innate immunity in the antiphospholipid syndrome: role of toll-like receptors in 
      endothelial cell activation by antiphospholipid antibodies.
PG  - 510-5
AB  - Antiphospholipid antibodies are mainly directed against beta 2 glycoprotein I 
      (beta2GPI), a plasma phospholipid-binding protein expressed on endothelial cells 
      of different anatomical localizations. Anti-beta2GPI antibodies recognize the 
      molecule on endothelial monolayers in vitro, and, once bound, might activate the 
      cells both in vitro and in vivo experimental models inducing a proinflammatory 
      and a procoagulant phenotype. Cell activation is associated with nuclear 
      factor-kappaB (NF-kappaB) translocation and with a signaling cascade comparable 
      to that triggered by the toll-like receptors (TLRs)-4. The cell membrane 
      receptor(s) for beta2GPI adhesion is still under investigation. It has been 
      suggested that beta2GPI might adhere through electrostatic interaction between 
      its cationic phospholipid binding site and anionic structures on the cell 
      membrane; however, binding to annexin II-the endothelial cell receptor for tissue 
      plasminogen activator-plays also a role. Because annexin II does not display any 
      transmembrane protein, it has been suggested that it requires a yet unknown 
      "adaptor" protein to signal the cells. Because of the molecular mimicry between 
      beta2GPI and viral/bacterial structures-the natural ligands for TLRs-antibodies 
      might cross-link the molecule associated to annexin II and TLR-4 eventually 
      triggering the signaling.
FAU - Meroni, P L
AU  - Meroni PL
AD  - Allergy, Clinical Immunology and Rheumatology Unit, Department of Internal 
      Medicine, University of Milan, IRCCS Istituto Auxologico Italiano, Via G. 
      Spagnoletto, 3, Milan 20149, Italy. pierluigi.meroni@unimi.it
FAU - Raschi, E
AU  - Raschi E
FAU - Testoni, C
AU  - Testoni C
FAU - Parisio, A
AU  - Parisio A
FAU - Borghi, M O
AU  - Borghi MO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PT  - Technical Report
PL  - Netherlands
TA  - Autoimmun Rev
JT  - Autoimmunity reviews
JID - 101128967
RN  - 0 (Antibodies, Antiphospholipid)
RN  - 0 (Glycoproteins)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (TLR4 protein, human)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Toll-Like Receptors)
RN  - 0 (beta 2-Glycoprotein I)
SB  - IM
MH  - Animals
MH  - Antibodies, Antiphospholipid/*immunology
MH  - Antiphospholipid Syndrome/*immunology
MH  - Endothelium/immunology
MH  - Glycoproteins/immunology
MH  - Humans
MH  - Immunity, Innate/*immunology
MH  - Membrane Glycoproteins/*immunology
MH  - Receptors, Cell Surface/*immunology
MH  - Signal Transduction/immunology
MH  - Toll-Like Receptor 4
MH  - Toll-Like Receptors
MH  - beta 2-Glycoprotein I
RF  - 39
EDAT- 2004/11/18 09:00
MHDA- 2005/04/20 09:00
CRDT- 2004/11/18 09:00
PHST- 2004/07/06 00:00 [accepted]
PHST- 2004/11/18 09:00 [pubmed]
PHST- 2005/04/20 09:00 [medline]
PHST- 2004/11/18 09:00 [entrez]
AID - S1568-9972(04)00106-5 [pii]
AID - 10.1016/j.autrev.2004.07.007 [doi]
PST - ppublish
SO  - Autoimmun Rev. 2004 Nov;3(7-8):510-5. doi: 10.1016/j.autrev.2004.07.007.