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1                                              AECA act by inducing the release of at least two endothe
2                                              AECA in patients with SLE or systemic vasculitis may con
3                                              AECA may be important in the mediation of humoral AR, ma
4                                              AECA positivity did not correlate with the presence of c
5                                              AECA stimulation of endothelial cell cultures increased
6                                              AECA was evaluated using an endothelial cell crossmatch
7                                              AECA(+) plasma also showed a similar pattern of reactivi
8                                              AECA(+) plasma reacted with multiple antigens expressed
9 ppear to react with multiple cell types, (2) AECA (+) plasma react with multiple antigens expressed o
10 6 of 8 AECA-positive SLE patients and 3 of 3 AECA-positive systemic vasculitis patients up-regulated
11                                        The 4 AECA-negative samples had no effect.
12                              IgG from 6 of 8 AECA-positive SLE patients and 3 of 3 AECA-positive syst
13  that at later time points (2-8 hours) after AECA addition, endothelium-derived interleukin-1 (IL-1)
14  levels of anti-endothelial cell antibodies (AECA) determined by an enzyme immunoassay are elevated d
15 ression of anti-endothelial cell antibodies (AECA) would have any predictive value for pregnancy outc
16             Antiendothelial cell antibodies (AECAs) are commonly detectable in diseases associated wi
17 ]) contain anti-endothelial cell antibodies (AECAs) capable of inducing endothelial cell apoptosis.
18 he role of anti-endothelial cell antibodies (AECAs) in allograft rejection.
19 for non-HLA antiendothelial cell antibodies (AECAs) in allograft rejection; however, evidence linking
20 AT1R-Ab) and anti-endothelial cell antibody (AECA).
21     We investigated the relationship between AECAs identified using donor-derived endothelial cell pr
22 obulin G (IgG) subtype determination of both AECAs and HLA antibodies bound to ECPs was performed usi
23 es against human vascular endothelial cells (AECA) were measured using a cellular ELISA developed fro
24 ls and other tissues to further characterize AECA induced by CMV infection.
25 elial cells treated with SSc sera containing AECAs.
26                           There are distinct AECA subsets in the sera of patients with limited SSc (w
27      These results suggest that the elevated AECA levels seen in CMV-infected transplant recipients m
28 obtained from each patient were examined for AECA and an endomyocardial biopsy was performed at regul
29 otein arrays to identify target antigens for AECAs isolated from the sera of recipients of kidney tra
30 ney recipients were tested pretransplant for AECAs and HLA-antibodies using flow cytometric crossmatc
31                                     All four AECAs were detected in 24% of pretransplant sera, and th
32 (23%) tested positive for donor-reactive IgG AECAs and had statistically higher SCr values and incide
33                                 IgM- and IgG-AECA were determined by cellular enzyme-linked immunosor
34                              Conversely, IgG-AECA levels were significantly higher in the serum of no
35 ion of donor-reactive immunoglobulin M (IgM) AECAs did not correlate with increased SCr or incidence
36                     The lowest levels of IgM-AECA in lupus pregnancy were associated with preeclampsi
37          A significantly higher level of IgM-AECA was found during normal pregnancy compared with tha
38 ith SLE did not have increased titers of IgM-AECA, but instead had levels similar to those found in h
39 tion, such as diminished levels of serum IgM-AECA detected in SLE patients, might contribute to the i
40 dual specific, (3) CMV-induced antibodies in AECA (+) plasma are primarily autoantibodies.
41 lograft rejection; however, evidence linking AECAs of known specificity to in vivo vascular injury is
42 leukin-1 (IL-1) accounted for the ability of AECA to increase leukocyte adhesion.
43 This response involves increased activity of AECA, suggesting a role of autoantibodies as a possible
44 en within very short times after addition of AECA (<30 minutes), endothelial cells released a distinc
45    The aim was to determine the incidence of AECA formation after transplantation and their associati
46          In a separate study, high levels of AECA are associated with higher frequency of humoral all
47   These results suggests that high levels of AECA produced during CMV infection may have a pathogenic
48                           The persistence of AECA positivity during the first year after transplantat
49 orrelation was found between the presence of AECA and humoral AR (P<0.015).
50           Here we examined the reactivity of AECA against endothelial cells and other tissues to furt
51 ium, but, in contrast to adhesion because of AECAs, this process did not require CXCR1/2, was not inh
52 o enhance PMN recruitment in the presence of AECAs suggests a mechanism whereby AECAs may augment tis
53 , anti-Scl-70 antibodies) contain subsets of AECAs that trigger distinct pathways of apoptosis and ge
54                            Each individual's AECA(+) plasma showed different patterns of reactivity a
55            IgG subclass determination showed AECAs to be enriched for IgG2 and IgG4, subclasses that
56 ents and in vivo histopathology suggest that AECAs activate the vascular endothelium, amplifying the
57  were no significant differences between the AECA (+) and (-) groups when examined for age, sex, and
58 the AECA (-) group compared with that in the AECA (+) group (89.8% vs. 71.0%, P<0.0004).
59 nsplantation was significantly better in the AECA (-) group compared with that in the AECA (+) group
60     We observed an identical mechanism using AECA IgG isolated directly from patients with SLE.
61         Of the 80 patients examined, 31 were AECA (+) and 49 patients were AECA (-).
62 mined, 31 were AECA (+) and 49 patients were AECA (-).
63 CAV when compared with the patients who were AECA (-) (25.8% vs. 14.3%, P<0.004).
64 esence of AECAs suggests a mechanism whereby AECAs may augment tissue injury during inflammatory resp

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