ライフサイエンスコーパス: HLA antigen

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 n allergic patients did not cross-react with HLA antigens.

5 f they are directed against mismatched donor HLA antigens.

6 d blood that were mismatched for two or more HLA antigens.

7 ic Ab (DSA) for one or more mismatched donor HLA antigens.

8 enic stimuli for antibody production against HLA antigens.

9 ersing AHR mediated by Ab specific for donor HLA antigens.

10 odies directed to either class I or class II HLA antigens.

11 valences and encourage laboratories to split HLA antigens.

12 pient pairs were discordant for one to three HLA antigens.

13 demonstrated specificity to mismatched donor HLA antigens.

14 rn following exposure to single and multiple HLA antigens.

15 ion of a transplant candidate's unacceptable HLA antigens.

16 e of donor-specific antibodies to HLA or non-HLA antigens.

17 same donor reduces the exposure to different HLA antigens.

18 s related to a reduced expression of class I HLA antigens.

19 ed in level of antibody reactivity to intact HLA antigens.

20 ested against iBeads coated only with intact HLA antigens.

21 ule that help to explain cross-reactivity of HLA antigens.

22 0% of them showed antibodies directed to non-HLA antigens.

23 respectively, with specific recombinant MHC/HLA antigens.

24 at inhibited Th alloreactivity against graft HLA antigens.

25 owerful in identifying epitopes shared among HLA antigens.

26 d basophils on stimulation with specific MHC/HLA antigens.

27 matching to exclude donors with unacceptable HLA antigens.

28 ated beads, possibly because it detected non-HLA antigens.

29 might have against human leukocyte antigen (HLA) antigens.

30 independent of the well-known association of HLA antigen (2-digit specificity) MMs with kidney graft

31 patients who developed "new" antibody to the HLA antigen (3.9%-8.6%) of the tetramer after transplant

32 eived cord blood that was mismatched for one HLA antigen (34 patients) or two antigens (116 patients)

33 ts with antibodies against beta2m-free HC of HLA antigens (88%, P=0.0056).

34 rmal antibody values as well as frequency of HLA antigen alleles were compared between patient and co

35 rols were tested for celiac disease-specific HLA antigen alleles; 13 of 22 TG6 IgA seropositive indiv

36 Registry data were used for derivation of HLA antigen and haplotype frequencies in a 1996 report.

37 ll and by method of identifying unacceptable HLA antigens and crossmatch techniques.

38 m 31 donors known to have antibodies against HLA antigens and from 16 antibody-negative controls were

39 ear evidence of improved definition of rarer HLA antigens and haplotypes, particularly among minoriti

40 with a self-eplet shared between immunizing HLA antigens and HLA antigens of the antibody producer.

41 xperimental filtration removed antibodies to HLA antigens and inhibited the accumulation of lipid pri

42 nsplantation by serologic typing for class I HLA antigens and low-resolution molecular typing for cla

43 correlation between the number of mismatched HLA antigens and the number of V beta elements involved.

44 filtrate EBV+ tumors bearing the appropriate HLA antigens and thereafter induce targeted regressions

45 e (HMO) and U937 on the levels of FcgammaRs, HLA antigens, and monokines, elutriated HMOs and U937 ce

46 s, detection of antibodies (Abs) against non-HLA antigens, and subjective scoring.

47 ssion have been found to underlie changes in HLA antigen, APM component, costimulatory molecule and t

48 These non-HLA antigens are classified as either alloantigens, such

49 HLA antigens are important targets of alloantibodies and

50 HLA antigens are polymorphic proteins expressed on donor

51 e impact when antibodies to both HLA and non-HLA antigens are present pretransplant.

52 ents may become sensitized to donor-specific HLA antigens as a result of previous antigenic exposures

53 Of a possible 74,514 individual HLA antigen assignments, 2.7% were discrepant.

54 frequency of discrepancies of the individual HLA antigen assignments.

55 Repeated mismatched HLA antigens between first and second transplant may be

56 Since HLA-antigen binding is the first step in initiating an i

57 We speculate that strong HLA-antigen binding likely protects against ME/CFS via e

58 mination of virus antigens; conversely, weak HLA-antigen binding may permit persistence of foreign an

59 where patients were considered sensitized to HLA antigens but did not have antibody before transplant

60 ic B cells in patients who are sensitized to HLA antigens but lacking detectable antibody abrogates a

61 because the donors expressed a diversity of HLA antigens, but was largely a result of the substrate-

62 th American white NIH blood donors typed for HLA antigens by the same molecular technique (HLA-DR15,

63 ion of unacceptable human leukocyte antigen (HLA) antigens by most advanced solid phase immunoassays

64 adaveric kidneys based on broader classes of HLA antigens, called cross-reactive groups (CREG).

65 d immune response factors, most specifically HLA antigen class I-restricted HIV-specific CD8 T cells,

66 somal regulation of tumor-associated peptide/HLA antigen complexes, and yield possible therapeutic so

67 Although alloantibodies against HLA antigens contribute to the pathogenesis of CAI, allo

68 sessing the variability in the expression of HLA antigens could have clinical monitoring and treatmen

69 entify a list of acceptable and unacceptable HLA antigens, could improve the access of highly sensiti

70 Some patients sensitized to HLA antigens do not have antibody present in serum speci

71 esence of serum anti-HLA antibodies to donor HLA antigens (donor-specific antibodies) and serum MHC c

72 A birth cohort of children with HLA antigen-DQB1-conferred susceptibility to type 1 diab

73 and that centers review the UNOS listing of HLA antigen equivalences and encourage laboratories to s

74 The United Network for Organ Sharing HLA antigen equivalences were applied to the data.

75 ndicate that preformed IgG Abs targeting non-HLA antigens expressed on glomerular endothelial cells a

76 in the regulatory mechanisms, which control HLA antigen expression and/or abnormalities in one or mo

77 nt cells as well as their role in changes in HLA antigen expression by malignant cells have been revi

78 igenetic modifications underlying changes in HLA antigen expression in malignant cells have been disc

79 Abnormalities in HLA antigen expression in malignant cells, which range i

80 enetic events associated with alterations in HLA antigen expression may be clinically relevant as, in

81 dy titers against Y chromosome-encoded minor HLA antigens fell and remained low, whereas titers again

82 Only 1 cellular target HLA antigen for the serum was expressed in 238 cases, 20

83 LA-A2 as a marker for the release of soluble HLA antigens from the donor, we established that recipie

84 ve cancer risk as outcome, not be focused on HLA antigen genetic markers, and be published in English

85 etween 2004 and 2010, 8676 newborns carrying HLA antigen genotypes associated with type 1 diabetes an

86 dated gliadine peptide and TG6 and performed HLA antigen genotyping in 150 consecutive patients with

87 gen heavy chain(s), mutations, which inhibit HLA antigen heavy chain transcription or translation, de

88 2)m) synthesis, loss of the gene(s) encoding HLA antigen heavy chain(s), mutations, which inhibit HLA

89 ypically matched kidneys with fewer than six HLA antigens identified had an 89% 1-year graft survival

90 globulin (Ig)G antibody to one or more donor HLA antigens in 49 patients treated with alternate-day,

91 t sex-mismatched, Y chromosome-encoded minor HLA antigens in association with chronic GVHD.

92 Co-STARs may have utility for other peptide-HLA antigens in cancer and other targets where antigen d

93 de novo antibodies against mismatched donor HLA antigens in kidney transplantation.

94 valence, and importance of antibodies to non-HLA antigens in late allograft injury are poorly charact

95 ght result in alloimmunisation stimulated by HLA antigens in seminal or cervicovaginal fluid.

96 pecific antibodies (DSA) against HLA and non-HLA antigens in the glomeruli and the tubulointerstitium

97 ese data challenge the current paradigm that HLA antigens, in particular HLA class II, are a single g

98 cess, which appears to be, at least in part, HLA antigen independent.

99 study addressed the question how mismatched HLA antigens induce specific antibodies in context with

100 Sensitization against HLA antigens is a growing problem in the field of pediat

101 hogenesis of CAI, alloantibodies against non-HLA antigens likely contribute as well.

102 Partially HLA antigen-matched allogeneic hematopoietic stem cell (

103 HLA alloimmunization necessitates the use of HLA antigen-matched platelets but requires a large plate

104 with severe Wiskott-Aldrich syndrome lacking HLA antigen-matched related or unrelated HSC donors (age

105 Engineered T cells caused cytotoxicity in HLA/antigen-matched tumors and induced IFN-gamma product

106 toimmunity directed at kidney-expressed, non-HLA antigens may also participate.

107 out differences in immunogenicity of various HLA antigens may help guide donor selection and identify

108 ough preliminary, these results suggest that HLA antigens may influence SARS-CoV-2 infection and clin

109 e a sequential kidney transplant, a repeated HLA antigen mismatch was not associated with a detriment

110 enal transplantation, functional status, and HLA antigen mismatch.

111 mandatory sharing of kidneys that have zero HLA antigens mismatched with specific patients on the wa

112 an male who received an ABO-compatible, five HLA antigen-mismatched kidney-pancreas transplant from a

113 UCB grafts (93%) were 1-2 HLA antigen-mismatched with the recipient and contained

114 ched related donors, 3.79 (P < .0001) with 2-HLA-antigen-mismatched related donors, 2.11 (P < .0001)

115 eference group, were 2.43 (P < .0001) with 1-HLA-antigen-mismatched related donors, 3.79 (P < .0001)

116 s in treatment failure were less striking: 1-HLA-antigen-mismatched relatives, 1.22 (P = not signific

117 elatives, 1.22 (P = not significant [NS]); 2-HLA-antigen-mismatched relatives, 1.81 (P < .0001); HLA-

118 hed unrelated donors, 1.39 (P = .002); and 1-HLA-antigen-mismatched unrelated donors, 1.63 (P = .002)

119 nrelated donors, and 3.33 (P < .0001) with 1-HLA-antigen-mismatched unrelated donors.

120 e specificities than can be accounted for by HLA antigen mismatches.

121 independent of the well-known association of HLA antigen MMs with graft survival.

122 including patient and donor risk factors and HLA antigen MMs.

123 ncluding the effect of noninherited maternal HLA antigens (NIMA) and double-unit cord blood transplan

124 of kidneys from siblings expressing paternal HLA antigens not inherited by the recipient (86 percent

125 of kidneys from siblings expressing maternal HLA antigens not inherited by the recipient than in reci

126 rvival is higher when the donor has maternal HLA antigens not inherited by the recipient than when th

127 sibling donors bearing maternal or paternal HLA antigens not inherited by the recipient.

128 e recipient than when the donor has paternal HLA antigens not inherited by the recipient.

129 ival advantage of grafts expressing maternal HLA antigens not inherited by the recipient.

130 y, loss of antibody to donor and third-party HLA antigens occurred in 89% and 19%, respectively, of p

131 comparisons were discrepant in at least one HLA antigen of six possible antigens per phenotype.

132 66%) B cells and a previous mismatch for the HLA antigen of the tetramer.

133 , and matching of CMV serological status and HLA antigens of donor and recipient.

134 low cytometry assessed the reactivity to non-HLA antigens of pretransplantation serum samples from 38

135 t shared between immunizing HLA antigens and HLA antigens of the antibody producer.

136 evidence of at least moderate antibodies to HLA antigens on cord units originally selected for trans

137 ass I or II donor-specific antibody bound to HLA antigens on the donor cell surface in their native c

138 pient pairs who differed by no more than one HLA antigen or allele, high-resolution class II HLA typi

139 -recipient pairs who were mismatched for two HLA antigens or alleles, high-resolution typing was used

140 ents with ESRD who were highly sensitized to HLA antigens (panel reactive antibody [PRA] > or =50% mo

141 IDs belonged to arachidonic acid pathway and HLA antigen processing pathway.

142 allocation policy and racial differences in HLA antigen profiles, using a Cox model for the time fro

143 While many of these non-HLA antigens remain poorly defined, the principal antige

144 Out of 17 class I HLA antigens represented by >1 allele in the LABScreen s

145 Whether reexposure to mismatched HLA antigens (RMM) in the setting of a negative crossmat

146 ated serum concentrations of soluble class I HLA antigens (S-HLA-I) with HLA allotypes in 82 unrelate

147 ells, and not as obviously influenced by the HLA antigen(s) on the stimulator cells.

148 The presence of mismatched HLA antigens seemed to affect the reconstitution kinetic

149 whether mismatched human leukocyte antigen (HLA) antigens should be avoided in subsequent renal tran

150 the detrimental impact of mismatch at other HLA antigens (such as DQ) and epitope mismatching on pos

151 lloimmunized both to neutrophil-specific and HLA antigens, suggesting that the transfusion of these p

152 Antibodies to 4/18 non-HLA antigens synergize with HLA donor-specific antibodie

153 e of DRB1 molecules, affecting the interface HLA-antigen-TCR B and potentially constituting the basis

154 preimplantation genetic diagnosis (PGD) and HLA antigen testing.

155 LAMatchmaker can identify certain mismatched HLA antigens that are zero-triplet mismatches to the pat

156 and anatomic roadmap of the most likely non-HLA antigens that can generate serological responses aft

157 des that share cryptic determinants with the HLA antigens that initially sensitized the patient.

158 riability in the immunogenicity of different HLA antigens that is impacted by the presence or absence

159 Testing System (KATS), that predicts class I HLA antigens that would be both "unacceptable" and "acce

160 Since the discovery of HLA antigens, the HLA system nomenclature and typing met

161 ddition, using actual patients' unacceptable HLA antigens, the number of compatible donors that would

162 ural antibodies to the heavy chains (HCs) of HLA antigens, the preparations were then tested against

163 n HLA allele imputation system that converts HLA antigens to alleles was developed to enhance the pre

164 .6% of the population) present no mismatched HLA antigens to be recognized by their offspring's immun

165 uring patient workup for transplantation and HLA antigens to which a patient is sensitized then be av

166 Families agreed to HLA antigen typing and transplantation if a matched sibl

167 8-year study, our analysis was based on the HLA antigens used for organ exchange (11 A locus antigen

168 at acquired tolerance to disparate unrelated HLA antigens was achieved.

169 t of IgG antibody directed to donor-specific HLA antigens was extremely uncommon and, furthermore, ha

170 dynamics of alloimmune responses directed at HLA antigens, we retrospectively evaluated data on anti-

171 patients with granulocytes matched only for HLA antigens will not be effective.

172 atches where available, or alternatively, no HLA antigens with more than five immunogenic triplet mis

173 ization of host alloreactivity to individual HLA antigens with sufficient sensitivity and specificity

174 ation of HLAMatchmaker identified additional HLA antigens with zero-triplet mismatches for 27 patient