Search

HLA‐C*16:116 differs from HLA‐C*16:01:01:01 by single‐nucleotide substitution at position 30. [ABSTRACT FROM AUTHOR]

A novel HLA-B allele, B*39:93, was identified in a French family. [ABSTRACT FROM AUTHOR]

A novel human leukocyte antigen-C ( HLA-C) allele, C*07:314, was identified in a French acute lymphoblastic leukemia patient. [ABSTRACT FROM AUTHOR]

HLA-C*07:01:126 differs from HLA-C*07:01:01:01 by one nucleotide substitution in codon 328 in exon 7., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-A*24:02:169 differs from HLA-A*24:02:01:01 by one nucleotide substitution in codon -23 in exon 1., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-C*01:262 differs from HLA-C*01:02:01:01 by one nucleotide substitution in codon 150 in exon 3., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-DPB1*1618:01 differs from HLA-DPB1*18:01:01:01 by one nucleotide substitution in codon 215 in exon 4., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-B*51:411 differs from HLA-B*51:01:01:01 by one nucleotide substitution in codon 235 in exon 4., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-A*26:247 differs from HLA-A*26:01:01:01 by one nucleotide substitution in codon 245 in exon 4., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-C*05:286 differs from HLA-C*05:01:01:02 by one nucleotide substitution in codon 283 in exon 5., (© 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-B*40:539 differs from HLA-B*40:01:01 by one nucleotide substitution in codon 46 in exon 2., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-DRB1*11:01:01:12N differs from HLA-DRB1*11:01:01:03 by one nucleotide substitution in intron 3 at position c.652+1G>C, hg19., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-C*12:384 differs from HLA-C*12:03:01:02 by one nucleotide substitution in codon 42 in exon 2., (© 2023 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

HLA-B*44:324:02 differs from HLA-B*44:324:01 by one nucleotide substitution in codon 99 in exon 3., (© 2023 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

HLA-C*05:282Q differs from HLA-C*05:01:01 by one nucleotide substitution in codon -24 in exon 1., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-DRB1*14:255 differs from HLA-DRB1*14:54:01 by one nucleotide substitution in codon 205 in exon 4., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-A*24:587 differs from HLA-A*24:02:01:01 by one nucleotide substitution in codon 220 in exon 4., (© 2023 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

HLA-C*03:552 differs from HLA-C*03:04:01:01 by one nucleotide substitution in codon 72 in exon 2., (© 2023 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-C*17:01:18 differs from HLA-C*17:01:01:05 by one nucleotide substitution in codon 18 in exon 2., (© 2022 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

HLA-A*11:422 differs from HLA-A*11:01:01:01 by one nucleotide substitution in codon 285 in exon 5., (© 2022 The Authors. HLA: Immune Response Genetics published by John Wiley & Sons Ltd.)

HLA-DQB1*02:200 differs from HLA-DQB1*02:02:01:02 by one nucleotide substitution in codon 148 in exon 3., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-B*44:03:62 differs from HLA-B*44:03:01:01 by one nucleotide substitution in codon 127 in exon 3., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Islet transplantation is a unique paradigm in organ transplantation, since multiple donors are required to achieve complete insulin-independence. Preformed or de novo Donor Specific Antibodies (DSA) may target one or several donor islets, which adds complexity to the analysis of their impact. Adult patients with type 1 diabetes transplanted with pancreatic islets between 2005 and 2018 were included in a single-center observational study. Thirty-two recipients with available sera tested by solid-phase assays for anti-HLA antibodies during their whole follow-up were analyzed. Twenty-five recipients were islet-transplantation-alone recipients, and 7 islet-after-kidney recipients. Seven recipients presented with DSA at any time during follow-up (two with preformed DSA only, one with preformed and de novo DSA, 4 with de novo DSA only). Only islet-transplantation-alone recipients presented with de novo DSA. Three clinical trajectories were identified according to: 1/the presence of preformed DSA, 2/early de novo DSA or 3/late de novo DSA. Only late de novo DSA were associated with unfavorable outcomes, depicted by a decrease of the β-score. Islet transplantation with preformed DSA, even with high MFI values, is associated with favorable outcomes in our experience. On the contrary, de novo DSA, and especially late de novo DSA, may be associated with allograft loss., (© 2022. The Author(s).)

HLA-A*30:02:28 differs from HLA-A*30:02:01:01 by one nucleotide substitution in codon 47 in exon 2., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-DQB1*06:385 differs from HLA-DQB1*06:07:01 by one nucleotide substitution in codon 70 in exon 2., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-C*07:01:101 differs from HLA-C*07:01:01:15 by one nucleotide substitution in codon 332 in exon 7., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-B*44:02:73 differs from HLA-B*44:02:01:01 by one nucleotide substitution in codon 89 in exon 2., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-A*24:538 differs from HLA-A*24:02:01:01 by one nucleotide substitution in codon -21 in exon 1., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

DQB1*03:417 differs from DQB1*03:01:01:01 by one nucleotide substitution at position 179 in exon 2., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

B*51:296 differs from B*51:01:01:01 by one nucleotide substitution at position 1030 in exon 6., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-B*35:29:03 differs from HLA-B*35:29:01 by one nucleotide substitution at position 374 in exon 2., (© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Enteroviruses are a frequent source of infection and among the most common central nervous system viral pathogens. Enteroviruses - in particular, the Coxsackie B viruses - are a known cause of myocarditis. Rituximab is a genetically engineered chimeric anti-CD20 monoclonal antibody. Many reports in the literature suggest a higher risk of infection following repeated rituximab therapy, including viral infection. However, observations of enterovirus-related myocarditis in the context of rituximab treatment are scarce. The authors describe the case of a patient with neuromyelitis optica spectrum disorder who developed severe and fatal enterovirus-related myocarditis after rituximab therapy with a difficult differential diagnosis of autoimmune or giant-cell myocarditis. This case highlights the importance of complete diagnostic workup in difficult cases of myocarditis, including endomyocardial biopsies., Competing Interests: Disclosure: The authors have no conflicts of interest to declare., (Copyright © 2021, Radcliffe Cardiology.)

HLA-A*11:376 differs from HLA-A*11:01:01:01 by one nucleotide substitution in codon 168 in exon 3., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-C*14:114 differs from C*14:02:01:01 by one nucleotide substitution at position 1077 in exon 7., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-DQB1*06:374 differs from HLA-DQB1*06:02:01:01 by one nucleotide substitution in codon 62 in exon 2., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

HLA-C*16:173 differs from HLA-C*16:01:01:01 by one nucleotide substitution in codon 36 in exon 2., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Objectives: Assessment of the adaptive immune response against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is crucial for studying long-term immunity and vaccine strategies. We quantified IFNγ-secreting T cells reactive against the main viral SARS-CoV-2 antigens using a standardised enzyme-linked immunospot assay (ELISpot)., Methods: Overlapping peptide pools built from the sequences of M, N and S viral proteins and a mix (MNS) were used as antigens. Using IFNγ T-CoV-Spot assay, we assessed T-cell and antibody responses in mild, moderate and severe SARS-CoV-2 patients and in control samples collected before the outbreak., Results: Specific T cells were assessed in 60 consecutive patients (mild, n  = 26; moderate, n  = 10; and severe patients, n  = 24) during their follow-up (median time from symptom onset [interquartile range]: 36 days [28;53]). T cells against M, N and S peptide pools were detected in n  = 60 (100%), n  = 56 (93.3%), n  = 55 patients (91.7%), respectively. Using the MNS mix, IFNγ T-CoV-Spot assay showed a specificity of 96.7% (95% CI, 88.5-99.6%) and a specificity of 90.3% (75.2-98.0%). The frequency of reactive T cells observed with M, S and MNS mix pools correlated with severity and with levels of anti-S1 and anti-RBD serum antibodies., Conclusion: IFNγ T-CoV-Spot assay is a reliable method to explore specific T cells in large cohorts of patients. This test may become a useful tool to assess the long-lived memory T-cell response after vaccination. Our study demonstrates that SARS-CoV-2 patients developing a severe disease achieve a higher adaptive immune response., Competing Interests: The authors declare no conflict of interest., (© 2020 The Authors. Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd on behalf of Australian and New Zealand Society for Immunology, Inc.)