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Data Sheet 1_HLA class, calcineurin inhibitor levels, and the risk of graft failure in kidney recipients with de novo donor-specific antibodies.pdf
Published 2024“…Introduction<p>De novo donor-specific HLA antibody (dnDSA) are associated with poor outcomes. …”
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Data Sheet 2_HLA class, calcineurin inhibitor levels, and the risk of graft failure in kidney recipients with de novo donor-specific antibodies.pdf
Published 2024“…Introduction<p>De novo donor-specific HLA antibody (dnDSA) are associated with poor outcomes. …”
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Data Sheet 1_Use of HLA desensitization in the management of renal transplant recipients in Europe.pdf
Published 2025“…As the degree of sensitization increases, the likelihood of finding a compatible organ decreases. Desensitization is the process of reducing recipient anti-HLA antibodies to acceptable levels to allow transplantation. …”
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All-Atom Simulations Reveal the Effect of Membrane Composition on the Signaling of the NKG2A/CD94/HLA‑E Immune Receptor Complex
Published 2024“…In this study, we employed all-atom molecular dynamics simulations to investigate the impact of different membrane compositions on the conformational dynamics of the NKG2A/CD94/HLA-E immune receptor complex, a key negative regulator of natural killer cell cytotoxic activity. …”
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ZIKV infection enriches the HLA Class I pathway in brain tumour cells.
Published 2025“…Normalised enrichment score (NES) denotes the degree to which the enrichment increased (+) or decreased (-). GSEA analysis significance is defined by p ≤ 0.05 and FDR ≤ 0.25. …”
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Data Sheet 1_Case Report: HLA-DRB1 04:01 found in a child with adenovirus type 2 -linked hepatitis.pdf
Published 2025“…Adeno-associated virus type 2 (AAV2) was identified as a cause, with most affected children having the HLA-DRB1 04:01 genotype. In this study, we hypothesized that HLA-DRB1 04:01 in the host may also be a potential predisposing factor of acute hepatitis caused by other viruses. …”
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Data Sheet 2_Case Report: HLA-DRB1 04:01 found in a child with adenovirus type 2 -linked hepatitis.pdf
Published 2025“…Adeno-associated virus type 2 (AAV2) was identified as a cause, with most affected children having the HLA-DRB1 04:01 genotype. In this study, we hypothesized that HLA-DRB1 04:01 in the host may also be a potential predisposing factor of acute hepatitis caused by other viruses. …”
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Image 1_Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.tiff
Published 2025“…Conversely, a stimulator of lysosome acidification/function, C381, decreased HLA-I expression. Lastly, we showed that in the presence of islet cells with defective autophagy, there is enhanced BDC2.5 T cell activation.…”
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Image 3_Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.tiff
Published 2025“…Conversely, a stimulator of lysosome acidification/function, C381, decreased HLA-I expression. Lastly, we showed that in the presence of islet cells with defective autophagy, there is enhanced BDC2.5 T cell activation.…”
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Image 4_Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.tif
Published 2025“…Conversely, a stimulator of lysosome acidification/function, C381, decreased HLA-I expression. Lastly, we showed that in the presence of islet cells with defective autophagy, there is enhanced BDC2.5 T cell activation.…”
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Image 2_Dysfunctional β-cell autophagy induces β-cell stress and enhances islet immunogenicity.tiff
Published 2025“…Conversely, a stimulator of lysosome acidification/function, C381, decreased HLA-I expression. Lastly, we showed that in the presence of islet cells with defective autophagy, there is enhanced BDC2.5 T cell activation.…”
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Image 6_Divergent B-cell and cytotoxic TNK cell activation signatures in HLA-B27-associated ankylosing spondylitis and acute anterior uveitis.jpeg
Published 2025“…Using cellular indexing of transcriptomes and epitopes (CITE-Seq) in a well-characterized cohort of 25 subjects—including AS (HLA-B27<sup>pos</sup>), AS+AAU (HLA-B27<sup>pos</sup>), AAU (HLA-B27<sup>pos</sup>), HCs (HLA-B27<sup>pos</sup>), and HCs (HLA-B27<sup>neg</sup>); N = 5/group—we identified transcriptomic differences at the single-cell level, along with differentially expressed cell surface markers. …”
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Image 9_Divergent B-cell and cytotoxic TNK cell activation signatures in HLA-B27-associated ankylosing spondylitis and acute anterior uveitis.jpeg
Published 2025“…Using cellular indexing of transcriptomes and epitopes (CITE-Seq) in a well-characterized cohort of 25 subjects—including AS (HLA-B27<sup>pos</sup>), AS+AAU (HLA-B27<sup>pos</sup>), AAU (HLA-B27<sup>pos</sup>), HCs (HLA-B27<sup>pos</sup>), and HCs (HLA-B27<sup>neg</sup>); N = 5/group—we identified transcriptomic differences at the single-cell level, along with differentially expressed cell surface markers. …”
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Data Sheet 1_Divergent B-cell and cytotoxic TNK cell activation signatures in HLA-B27-associated ankylosing spondylitis and acute anterior uveitis.docx
Published 2025“…Using cellular indexing of transcriptomes and epitopes (CITE-Seq) in a well-characterized cohort of 25 subjects—including AS (HLA-B27<sup>pos</sup>), AS+AAU (HLA-B27<sup>pos</sup>), AAU (HLA-B27<sup>pos</sup>), HCs (HLA-B27<sup>pos</sup>), and HCs (HLA-B27<sup>neg</sup>); N = 5/group—we identified transcriptomic differences at the single-cell level, along with differentially expressed cell surface markers. …”
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Image 5_Divergent B-cell and cytotoxic TNK cell activation signatures in HLA-B27-associated ankylosing spondylitis and acute anterior uveitis.jpeg
Published 2025“…Using cellular indexing of transcriptomes and epitopes (CITE-Seq) in a well-characterized cohort of 25 subjects—including AS (HLA-B27<sup>pos</sup>), AS+AAU (HLA-B27<sup>pos</sup>), AAU (HLA-B27<sup>pos</sup>), HCs (HLA-B27<sup>pos</sup>), and HCs (HLA-B27<sup>neg</sup>); N = 5/group—we identified transcriptomic differences at the single-cell level, along with differentially expressed cell surface markers. …”
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Data Sheet 2_Divergent B-cell and cytotoxic TNK cell activation signatures in HLA-B27-associated ankylosing spondylitis and acute anterior uveitis.xlsx
Published 2025“…Using cellular indexing of transcriptomes and epitopes (CITE-Seq) in a well-characterized cohort of 25 subjects—including AS (HLA-B27<sup>pos</sup>), AS+AAU (HLA-B27<sup>pos</sup>), AAU (HLA-B27<sup>pos</sup>), HCs (HLA-B27<sup>pos</sup>), and HCs (HLA-B27<sup>neg</sup>); N = 5/group—we identified transcriptomic differences at the single-cell level, along with differentially expressed cell surface markers. …”
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Image 3_Divergent B-cell and cytotoxic TNK cell activation signatures in HLA-B27-associated ankylosing spondylitis and acute anterior uveitis.jpeg
Published 2025“…Using cellular indexing of transcriptomes and epitopes (CITE-Seq) in a well-characterized cohort of 25 subjects—including AS (HLA-B27<sup>pos</sup>), AS+AAU (HLA-B27<sup>pos</sup>), AAU (HLA-B27<sup>pos</sup>), HCs (HLA-B27<sup>pos</sup>), and HCs (HLA-B27<sup>neg</sup>); N = 5/group—we identified transcriptomic differences at the single-cell level, along with differentially expressed cell surface markers. …”
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Data Sheet 3_Divergent B-cell and cytotoxic TNK cell activation signatures in HLA-B27-associated ankylosing spondylitis and acute anterior uveitis.xlsx
Published 2025“…Using cellular indexing of transcriptomes and epitopes (CITE-Seq) in a well-characterized cohort of 25 subjects—including AS (HLA-B27<sup>pos</sup>), AS+AAU (HLA-B27<sup>pos</sup>), AAU (HLA-B27<sup>pos</sup>), HCs (HLA-B27<sup>pos</sup>), and HCs (HLA-B27<sup>neg</sup>); N = 5/group—we identified transcriptomic differences at the single-cell level, along with differentially expressed cell surface markers. …”
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Image 7_Divergent B-cell and cytotoxic TNK cell activation signatures in HLA-B27-associated ankylosing spondylitis and acute anterior uveitis.jpg
Published 2025“…Using cellular indexing of transcriptomes and epitopes (CITE-Seq) in a well-characterized cohort of 25 subjects—including AS (HLA-B27<sup>pos</sup>), AS+AAU (HLA-B27<sup>pos</sup>), AAU (HLA-B27<sup>pos</sup>), HCs (HLA-B27<sup>pos</sup>), and HCs (HLA-B27<sup>neg</sup>); N = 5/group—we identified transcriptomic differences at the single-cell level, along with differentially expressed cell surface markers. …”