Anti-heparin antibodies: part of the repertoire of anti-endothelial cell antibodies (AECA)

Harper, Lisa R.; Savage, C. O. S.

doi:10.1191/096120398678919859

Cited by 8 publications

(2 citation statements)

References 50 publications

(40 reference statements)

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“…40 Still unknown are the anionic structures of the EC membrane that are involved in such a binding. Since heparan sulphate (HS) -the major proteoglycan of the vascular endothelium -constitutes the majority of the endothelial anionic sites, 41 we investigated whether it represented the corresponding structure for the b2GPI PL-binding site. Figure 3 shows that heparitinase I -an enzyme able to cleave speci cally the a-N-acetyl-D-glycosaminidic linkage in HSsigni cantly downregulates the b2GPI binding treatment of HUVEC up to 60% at the highest enzyme concentrations.…”

Section: Expression Of B2gpi On Hbmec Membranementioning

confidence: 99%

Endothelium and the brain in CNS lupus

Meroni

Tincani

Sepp

et al. 2003

Lupus

101

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Central nervous system (CNS) involvement in systemic lupus erythematosus (SLE) is common and results in different clinical manifestations. Several pathogenic mechanisms have been suggested to play a role in determining such a variety of clinical symptoms. The thrombophilic state associated to the presence of antiphospholipid antibodies has been suggested to be responsible for a noninflammatory vasculopathy which causes clear ischaemic events as well as alterations of the cerebral microcirculation that are likely associated to seizures, cognitive dysfunction or psychosis. Although less frequent, a true vasculitic process affecting cerebral circulation has also been reported. In both cases, brain endothelium does represent the target of the pathogenic mechanisms. Brain endothelial cells display peculiar functional and phenotypical characteristics in comparison with endothelial cells from other anatomical districts, raising the possibility that this might be the reason for its susceptibility in lupus disease. We review and present data suggesting that a higher and firmer expression of beta 2 glycoprotein I on endothelial cell membranes can be responsible for a selective damage/activation by circulating anti-beta 2 glycoprotein I, and that antiendothelial cell antibodies crossreact with brain endothelium and in some cases, specifically bind brain endothelial cells only in lupus patients with central nervous involvement.

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Section: Expression Of B2gpi On Hbmec Membranementioning

confidence: 99%

Endothelium and the brain in CNS lupus

Meroni

Tincani

Sepp

et al. 2003

Lupus

101

View full text Add to dashboard Cite

show abstract

“…27 As AHA correlate with AECA activity, these antibodies could be considered to be part of the AECA repertoire. 28 Furthermore, it has been shown that autoantibodies to heparan sulphate may contribute to vascular injury via CDC mechanisms in MRL/lpr/lpr mice; 29 …”

Section: Activation Of Endothelial Cellsmentioning

confidence: 99%