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we decrease » _ decrease (Expand Search), a decrease (Expand Search), nn decrease (Expand Search)
hla we » hla e (Expand Search)
marked decrease » marked increase (Expand Search)
we decrease » _ decrease (Expand Search), a decrease (Expand Search), nn decrease (Expand Search)
hla we » hla e (Expand Search)
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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“…Whether this observation applies to both HLA class I and II dnDSA remains unclear.</p>Methods<p>We studied 1236 consecutive kidney recipients who had routine anti-HLA antibody surveillance post-transplant.…”
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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“…Whether this observation applies to both HLA class I and II dnDSA remains unclear.</p>Methods<p>We studied 1236 consecutive kidney recipients who had routine anti-HLA antibody surveillance post-transplant.…”
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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“…Understanding how membrane composition influences the dynamics and function of transmembrane proteins is crucial for the comprehensive elucidation of cellular signaling mechanisms and the development of targeted therapeutics. 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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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. …”