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468 results for “HLA”
Screen of A6,B7,1G4 TCRs against a library of HLA-A*02:01 MHC-I peptides from the human exome
<p>T2 cells expressing a library of off targets (derived from A6 and B7 binding motifs in Hausmann 1999) are co-cultured with A6, B7 or1G4 expressing T cells (from a non-A2 donor). Minigenes from surviving cells are amplified and sequenced.</p>
KIR3DL1 allotype binding to HLA by Luminex (W632 nomalised values).
<p>HLA-I recognition by KIR3DL1 allotypes was assessed through binding of KIR3DL1 tetramers to beads coated with a panel of 100 different HLA-A, -B, and -C molecules (LABScreen HLA Class I Single Antigen; One Lambda). PE-conjugated KIR3DL1 tetramer (5 µg per test) was incubated with beads for 30 min at room temperature in the dark in 300 mM of phosphate-buffered NaCl (PBS-300) with 5% fetal calf serum (AusGeneX). The beads were then washed three times in PBS-300 with 0.05% Tween 20 and resuspended in PBS-300. Binding was measured on a Luminex platform (LABScan 100; One Lambda) through identification of the individual HLA allotypes via unique bead labeling and detection of tetramer fluorescence intensity on each bead set. Normalized fluorescence values for analysis were obtained using the HLA Fusion software suite (One Lambda) that subtracted background values using the following formula:</p> <p>(<em>S</em>#<em>N</em> − <em>S</em><em>N</em><em>C</em> <em>b</em><em>e</em><em>a</em><em>d</em>) − (<em>B</em><em>G</em>#<em>N</em> − <em>B</em><em>G</em><em>N</em><em>C</em> <em>b</em><em>e</em><em>a</em><em>d</em>), </p> <p>where <em>S</em>#<em>N</em> is the sample-specific fluorescence value (trimmed mean) for bead #<em>N</em>, <em>SNC bead</em> is the sample-specific fluorescence value for the negative control (nude) bead, <em>BG</em>#<em>N</em> is the background negative control fluorescence value for bead #<em>N</em>, and <em>BGNC bead</em> is the background negative control fluorescence value for negative control bead. To obtain binding values for each HLA-I, mean fluorescence intensity (MFI) values for an isotype control (a PE-conjugated IgG) were subtracted from the raw values obtained for each experiment, and recognition was assessed as being higher than that of the tetramer to beads without conjugated HLA-I. MFI values were normalized to the highest value for each experiment and also provided averaged over three experiments.</p>
HLA epitopic mismatch and risk of developing Donor Specific Antibodies in pediatric kidney transplantation
<p>The aim of this study was to evaluate the correlation between epitopic HLA mismatches and the risk of developing DSA in pediatric kidney recipients. There are very few publications concerning epitope HLA mismatch in pediatric kidney transplantation although this topic has been growing in scientific articles in recent years and is promising in adult recipients. The majority of children with chronic renal failure will require multiple kidney transplants during their lifetime and it is therefore important that we can limit the risk of antibody development in order to give them the best chance of survival for their future kidney transplants.</p>
Data for: Endo-lysosomal assembly variations among Human Leukocyte Antigen class I (HLA-I) allotypes
<p>The extreme polymorphisms of HLA-I proteins enable the presentation of diverse peptides to cytotoxic T lymphocytes (CTL). The canonical endoplasmic reticulum (ER) HLA-I assembly pathway enables presentation of cytosolic peptides, but effective intracellular surveillance requires multi-compartmental antigen sampling. Endo-lysosomes are generally sites of HLA class II assembly, but human monocytes and monocyte-derived dendritic cells (moDCs) also contain significant reserves of endo-lysosomal HLA-I molecules. We hypothesized variable influences of HLA-I polymorphisms upon outcomes of endo-lysosomal trafficking, as the stabilities and peptide occupancies of cell surface HLA-I are variable. Consistent with this model, when the endo-lysosomal pH of moDCs is disrupted, HLA-B allotypes display varying propensities for reductions in surface expression, with HLA-B*08:01 or HLA-B*35:01 being among the most resistant or sensitive respectively, among eight tested HLA-B allotypes. Perturbations of moDC endo-lysosomal pH result in redistribution of HLA-B*35:01, but not HLA-B*08:01, to LAMP1+ compartments and increase HLA-B*35:01 peptide receptivity. These findings reveal the intersection of the vacuolar cross-presentation pathway with a constitutive assembly pathway for some HLA-B allotypes. Notably, cross-presentation of epitopes derived from two soluble antigens was also more efficient for B*35:01 compared to B*08:01, even when matched for T cell response sensitivity, and more affected by cathepsin inhibition. Thus, HLA-I polymorphisms dictate the degree of endo-lysosomal assembly, which can supplement ER assembly for constitutive HLA-I expression and increase the efficiency of cross-presentation.</p>
HLA class I Sanger sequences data of Honduras HIV cohort
<p>HLA polymorphisms represent the strongest genetic modifier of HIV disease progression. Diverse HLA distribution can lead to distinct HIV control landscapes at the population level. We aimed to describe HLA allele and haplotype frequencies (linkage disequilibrium, LD), CCR5-Δ32 frequency and the impact of these variants on HIV disease outcome. HLA class I (cI) loci were typed at 4-digit resolution, and CCR5 variants were determined in 402 HIV clade B-infected, ART-naïve individuals from Honduras. HLA LD were assessed using Fisher's exact test. Using univariable and multivariable analyses we evaluated HLA associations with HIV pVL and CD4 counts. We did not find any effect on HIV control between CCR5 genotypes. Previously defined HLA associations were found: <em>B*57:01/03</em>, <em>B*42:01</em>, <em>A*25:01</em> and <em>C*12:03</em> (protective), and <em>B*53:01</em> and <em>A*68:01</em> (risk). Being consistent with our previous research in a Mesoamerican HIV cohort, Amerindian <em>B*35:12</em> was associated to poor HIV control. Other HLA-HIV associations not previously described were <em>C*03:04</em> and <em>B*08:01</em> that were associated with higher pVL. Overall, this first report highlights the immunogenetic uniqueness admixture of the Honduras population that express Amerindian, Caucasian and African HLA subtypes. These findings not only support this cohort as ideal for identifying HLA correlates of HIV control but also may improve future research regarding allotransplantation and disease association.</p>
T Cell Receptor Immunotherapy Targeting MAGE-A3 for Patients With Metastatic Cancer Who Are HLA-DP0401 Positive
ClinicalTrials.gov study NCT02111850. IPD Sharing: NO. Countries: 1. Publications: 3.
Comparison of Tacrolimus Extended-Release (Envarsus XR) to Tacrolimus Immediate-Release in Human Leukocyte Antigen (HLA) Sensitized Kidney Transplant Recipients
ClinicalTrials.gov study NCT04225988. IPD Sharing: NO. Countries: 1. Publications: 9.
A Pilot Study of Genetically Engineered NY-ESO-1 Specific NY-ESO-1ᶜ²⁵⁹T in HLA-A2+ Patients With Synovial Sarcoma
ClinicalTrials.gov study NCT01343043. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Effects of Mycophenolate Mofetil (MMF) On Anti-HLA (Human Leukocyte Antigen)Antibody Levels In Patients Awaiting Cadaveric Renal Transplant.
ClinicalTrials.gov study NCT00446459. IPD Sharing: Not stated. Countries: 1. Publications: 9.
Vaccine Therapy in Treating Patients With Stage IV HLA-A2 and HER2 Positive Breast or Ovarian Cancer Receiving Trastuzumab
ClinicalTrials.gov study NCT00194714. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Rituximab in Renal Allograft Recipients Who Develop Early De Novo Anti-HLA Alloantibodies
ClinicalTrials.gov study NCT00307125. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Assessment of the Anti-inflammatory Effects of Norflo Oro in Acute Relapses of HLA-B27 Associated Autoimmune Uveitis
ClinicalTrials.gov study NCT03584724. IPD Sharing: NO. Countries: 1. Publications: 4.
Immunotherapy of HLA-A2 Positive Stage II-IV Melanoma Patients
ClinicalTrials.gov study NCT01308294. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Reduced Intensity, Partially HLA Mismatched BMT to Treat Hematologic Malignancies
ClinicalTrials.gov study NCT01203722. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Allogeneic HCT With HLA-matched Donors : a Phase II Randomized Study Comparing 2 Nonmyeloablative Conditionings
ClinicalTrials.gov study NCT00603954. IPD Sharing: Not stated. Countries: 2. Publications: 2.
HLA-Identical Sibling Renal Transplant Tolerance
ClinicalTrials.gov study NCT00619528. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Safety Trial of NK DLI From 6/6 HLA Matched Family Member Following Nonmyeloablative ASCT
ClinicalTrials.gov study NCT00586690. IPD Sharing: Not stated. Countries: 1. Publications: 1.
A Study to Learn How Safe and Tolerable Vonsetamig is in Adult Patients With Chronic Kidney Disease (CKD) Who Need Kidney Transplantation and Are Highly Sensitized to Human Leukocyte Antigen (HLA)
ClinicalTrials.gov study NCT05092347. IPD Sharing: YES. Countries: 1. Publications: 0.
Selective Depletion of CD45RA+ T Cells From Allogeneic Peripheral Blood Stem Cell Grafts From HLA-Matched Related and Unrelated Donors in Preventing GVHD
ClinicalTrials.gov study NCT02220985. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Administering Peripheral Blood Lymphocytes Transduced With a Murine T-Cell Receptor Recognizing the G12D Variant of Mutated RAS in HLA-A*11:01 Patients
ClinicalTrials.gov study NCT03745326. IPD Sharing: YES. Countries: 1. Publications: 3.
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OpenNeuro
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