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1 e HLA mismatched (4.6+/-1.2 of the six major HLA antigens).
2 ing or a sibling with a mismatch of a single HLA antigen.
3 unrelated donors were mismatched for >/= one HLA antigen.
4 enic stimuli for antibody production against HLA antigens.
5 ersing AHR mediated by Ab specific for donor HLA antigens.
6 odies directed to either class I or class II HLA antigens.
7 same donor reduces the exposure to different HLA antigens.
8 valences and encourage laboratories to split HLA antigens.
9 pient pairs were discordant for one to three HLA antigens.
10 demonstrated specificity to mismatched donor HLA antigens.
11 rn following exposure to single and multiple HLA antigens.
12 s related to a reduced expression of class I HLA antigens.
13 ed in level of antibody reactivity to intact HLA antigens.
14 ested against iBeads coated only with intact HLA antigens.
15 ion of a transplant candidate's unacceptable HLA antigens.
16 0% of them showed antibodies directed to non-HLA antigens.
17 at inhibited Th alloreactivity against graft HLA antigens.
18 owerful in identifying epitopes shared among HLA antigens.
19 matching to exclude donors with unacceptable HLA antigens.
20 ated beads, possibly because it detected non-HLA antigens.
21 f they are directed against mismatched donor HLA antigens.
22 d blood that were mismatched for two or more HLA antigens.
23 ic Ab (DSA) for one or more mismatched donor HLA antigens.
24 might have against human leukocyte antigen (HLA) antigens.
25 independent of the well-known association of HLA antigen (2-digit specificity) MMs with kidney graft
26 patients who developed "new" antibody to the HLA antigen (3.9%-8.6%) of the tetramer after transplant
27 eived cord blood that was mismatched for one HLA antigen (34 patients) or two antigens (116 patients)
29 rmal antibody values as well as frequency of HLA antigen alleles were compared between patient and co
30 rols were tested for celiac disease-specific HLA antigen alleles; 13 of 22 TG6 IgA seropositive indiv
31 Registry data were used for derivation of HLA antigen and haplotype frequencies in a 1996 report.
33 m 31 donors known to have antibodies against HLA antigens and from 16 antibody-negative controls were
34 ear evidence of improved definition of rarer HLA antigens and haplotypes, particularly among minoriti
35 with a self-eplet shared between immunizing HLA antigens and HLA antigens of the antibody producer.
36 xperimental filtration removed antibodies to HLA antigens and inhibited the accumulation of lipid pri
37 nsplantation by serologic typing for class I HLA antigens and low-resolution molecular typing for cla
38 correlation between the number of mismatched HLA antigens and the number of V beta elements involved.
39 filtrate EBV+ tumors bearing the appropriate HLA antigens and thereafter induce targeted regressions
40 e (HMO) and U937 on the levels of FcgammaRs, HLA antigens, and monokines, elutriated HMOs and U937 ce
42 ssion have been found to underlie changes in HLA antigen, APM component, costimulatory molecule and t
46 ents may become sensitized to donor-specific HLA antigens as a result of previous antigenic exposures
50 where patients were considered sensitized to HLA antigens but did not have antibody before transplant
51 ic B cells in patients who are sensitized to HLA antigens but lacking detectable antibody abrogates a
52 because the donors expressed a diversity of HLA antigens, but was largely a result of the substrate-
53 th American white NIH blood donors typed for HLA antigens by the same molecular technique (HLA-DR15,
54 ion of unacceptable human leukocyte antigen (HLA) antigens by most advanced solid phase immunoassays
56 d immune response factors, most specifically HLA antigen class I-restricted HIV-specific CD8 T cells,
57 somal regulation of tumor-associated peptide/HLA antigen complexes, and yield possible therapeutic so
59 entify a list of acceptable and unacceptable HLA antigens, could improve the access of highly sensiti
61 esence of serum anti-HLA antibodies to donor HLA antigens (donor-specific antibodies) and serum MHC c
63 and that centers review the UNOS listing of HLA antigen equivalences and encourage laboratories to s
65 in the regulatory mechanisms, which control HLA antigen expression and/or abnormalities in one or mo
66 nt cells as well as their role in changes in HLA antigen expression by malignant cells have been revi
67 igenetic modifications underlying changes in HLA antigen expression in malignant cells have been disc
69 enetic events associated with alterations in HLA antigen expression may be clinically relevant as, in
70 dy titers against Y chromosome-encoded minor HLA antigens fell and remained low, whereas titers again
72 LA-A2 as a marker for the release of soluble HLA antigens from the donor, we established that recipie
73 ve cancer risk as outcome, not be focused on HLA antigen genetic markers, and be published in English
74 dated gliadine peptide and TG6 and performed HLA antigen genotyping in 150 consecutive patients with
75 gen heavy chain(s), mutations, which inhibit HLA antigen heavy chain transcription or translation, de
76 2)m) synthesis, loss of the gene(s) encoding HLA antigen heavy chain(s), mutations, which inhibit HLA
77 ypically matched kidneys with fewer than six HLA antigens identified had an 89% 1-year graft survival
78 globulin (Ig)G antibody to one or more donor HLA antigens in 49 patients treated with alternate-day,
81 valence, and importance of antibodies to non-HLA antigens in late allograft injury are poorly charact
84 study addressed the question how mismatched HLA antigens induce specific antibodies in context with
88 with severe Wiskott-Aldrich syndrome lacking HLA antigen-matched related or unrelated HSC donors (age
89 Engineered T cells caused cytotoxicity in HLA/antigen-matched tumors and induced IFN-gamma product
91 out differences in immunogenicity of various HLA antigens may help guide donor selection and identify
92 e a sequential kidney transplant, a repeated HLA antigen mismatch was not associated with a detriment
94 mandatory sharing of kidneys that have zero HLA antigens mismatched with specific patients on the wa
95 an male who received an ABO-compatible, five HLA antigen-mismatched kidney-pancreas transplant from a
97 ched related donors, 3.79 (P < .0001) with 2-HLA-antigen-mismatched related donors, 2.11 (P < .0001)
98 eference group, were 2.43 (P < .0001) with 1-HLA-antigen-mismatched related donors, 3.79 (P < .0001)
99 s in treatment failure were less striking: 1-HLA-antigen-mismatched relatives, 1.22 (P = not signific
100 elatives, 1.22 (P = not significant [NS]); 2-HLA-antigen-mismatched relatives, 1.81 (P < .0001); HLA-
101 hed unrelated donors, 1.39 (P = .002); and 1-HLA-antigen-mismatched unrelated donors, 1.63 (P = .002)
106 ncluding the effect of noninherited maternal HLA antigens (NIMA) and double-unit cord blood transplan
107 of kidneys from siblings expressing paternal HLA antigens not inherited by the recipient (86 percent
108 of kidneys from siblings expressing maternal HLA antigens not inherited by the recipient than in reci
109 rvival is higher when the donor has maternal HLA antigens not inherited by the recipient than when th
113 y, loss of antibody to donor and third-party HLA antigens occurred in 89% and 19%, respectively, of p
118 evidence of at least moderate antibodies to HLA antigens on cord units originally selected for trans
119 pient pairs who differed by no more than one HLA antigen or allele, high-resolution class II HLA typi
120 -recipient pairs who were mismatched for two HLA antigens or alleles, high-resolution typing was used
121 ents with ESRD who were highly sensitized to HLA antigens (panel reactive antibody [PRA] > or =50% mo
123 allocation policy and racial differences in HLA antigen profiles, using a Cox model for the time fro
125 ated serum concentrations of soluble class I HLA antigens (S-HLA-I) with HLA allotypes in 82 unrelate
128 whether mismatched human leukocyte antigen (HLA) antigens should be avoided in subsequent renal tran
129 lloimmunized both to neutrophil-specific and HLA antigens, suggesting that the transfusion of these p
131 LAMatchmaker can identify certain mismatched HLA antigens that are zero-triplet mismatches to the pat
132 and anatomic roadmap of the most likely non-HLA antigens that can generate serological responses aft
133 des that share cryptic determinants with the HLA antigens that initially sensitized the patient.
134 riability in the immunogenicity of different HLA antigens that is impacted by the presence or absence
135 Testing System (KATS), that predicts class I HLA antigens that would be both "unacceptable" and "acce
136 ddition, using actual patients' unacceptable HLA antigens, the number of compatible donors that would
137 ural antibodies to the heavy chains (HCs) of HLA antigens, the preparations were then tested against
138 .6% of the population) present no mismatched HLA antigens to be recognized by their offspring's immun
139 uring patient workup for transplantation and HLA antigens to which a patient is sensitized then be av
140 8-year study, our analysis was based on the HLA antigens used for organ exchange (11 A locus antigen
142 t of IgG antibody directed to donor-specific HLA antigens was extremely uncommon and, furthermore, ha
144 atches where available, or alternatively, no HLA antigens with more than five immunogenic triplet mis
145 ization of host alloreactivity to individual HLA antigens with sufficient sensitivity and specificity
146 ation of HLAMatchmaker identified additional HLA antigens with zero-triplet mismatches for 27 patient
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