1 recurrence is in most cases associated with
anti-phospholipid A2 receptor antibodies (antiPLA2R).
2 The combined presence of
anti-phospholipid Ab (aPL) and thrombosis is recognized
3 h IgG from patients with PM alone (VT-/PM+),
anti-phospholipid Ab-positive patients without APS, or h
4 fusion of both anti-beta2-glycoprotein I and
anti-phospholipid Ab.
5 e performed experiments to determine whether
anti-phospholipid Abs can also reconstitute I/R injury a
6 We conclude that
anti-phospholipid Abs can bind to tissues subjected to I
7 Because
anti-phospholipid Abs have been shown to mediate fetal g
8 The presence in these mice of
anti-phospholipid Abs reacting with beta2-glycoprotein I
9 an auto-antibodies (B3/33H11, anti-DNA; UK4,
anti-phospholipid)
and six related hybrids have been clo
10 man autoantibodies (B3/33H11, anti-DNA; UK4,
anti-phospholipid)
and six related hybrids have been clo
11 ti-platelet factor 4/polyanion (anti-PF4/P),
anti-phospholipid,
anti-phosphatidylserine, anti-myelope
12 Anti-phospholipid antibodies (APA) are autoantibodies kn
13 ma levels (P < 0.0001) and low occurrence of
anti-phospholipid antibodies in lupus patients (4.8% ant
14 apoptotic cells are procoagulant and whether
anti-phospholipid antibodies influence this.
15 A subgroup of thrombotic patients with
anti-phospholipid antibodies specifically blocked the ox
16 ospholipid-bound form is the target for most
anti-phospholipid antibodies that are associated with re
17 Anti-phospholipid antibodies that block this process wou
18 ith anti-cardiolipin antibodies, a subset of
anti-phospholipid antibodies, bound to sulfatide-bound b
19 ertain autoantibodies, such as anti-NMDAR or
anti-phospholipid antibodies, promote CNS lupus.
20 systemic lupus erythematosus (SLE) who have
anti-phospholipid antibodies, we addressed whether apopt
21 of these blebs can induce the production of
anti-phospholipid antibodies, which might also enhance t
22 licated in haemostasis and the production of
anti-phospholipid antibodies.
23 sulfatides and thereby becomes a target for
anti-phospholipid antibodies.
24 beta2GPI plasma levels and the occurrence of
anti-phospholipid antibodies.
25 wn, but also sulfatides are targets for most
anti-phospholipid antibodies.
26 s that occur in some lupus patients who have
anti-phospholipid antibodies.
27 ified from the plasma of three patients with
anti-phospholipid antibody syndrome, but not IgG from no
28 bute to some of the clinical symptoms of the
anti-phospholipid antibody syndrome.
29 Anti-phospholipid autoantibodies (aPL) are associated wi
30 e by using the conjugated diene to exert its
anti-phospholipid autoxidation function and shields plas
31 Anti-phospholipid mAbs inhibited PBMC HIV-1 infection in
32 We report that four human
anti-phospholipid monoclonal antibodies (mAbs) (PGN632,
33 The combined presence of
anti-phospholipid (
PL) Ab, including lupus anticoagulant
34 romes such as myocardial infarction, sepsis,
anti-phospholipid syndrome and sickle-cell disease.
35 VTE and arterial thrombosis (associated with
anti-phospholipid syndrome) were reported in 0.86% (95%
36 gulant activity similar to those observed in
anti-phospholipid syndrome, suggesting that they may hav
37 in immune regulation, possibly including the
anti-phospholipid syndrome.
38 target of autoantibodies in humans with the
anti-phospholipid syndrome.
39 uate the risk of thrombosis in patients with
anti-phospholipid syndrome.