HLA‐B*07:355 differs from B*07:02:01:01 by one nucleotide substitution at position 916 in exon 5.

C*15:203 differs from C*15:02:01:01 by one nucleotide substitution at position 142 in exon 2.

Nucleotide substitution in codon 304 of HLA‐A*02:07:01:01 or HLA‐A*02:07:01:02 results in a novel allele, HLA‐A*02:935 .

B*15:547 differs from B*15:01:01:04 by one nucleotide substitution at position 1051 in exon 7.

DQB1*06:352 differs from DQB1*06:03:01:01 by one nucleotide substitution at position 668 in exon 4.

A*32:134 differs from A*32:01:01:01 by one nucleotide substitution at position 925 in exon 5.

DRB1*15:175 differs from DRB1*15:01:01:02 by one nucleotide substitution at position 233 in exon 2.

A*29:141 differs from A*29:02:01:01 by one nucleotide substitution at position 275 in exon 2.

HLA‐B*53:62 differs from HLA‐B*53:01:01:01 by seven nucleotide substitutions in six codons in exon 3.

C*07:841 differs from C*07:06:01:01 by one nucleotide substitution at position 845 in exon 4.

HLA‐DQB1*05:02:12 differs from HLA‐DQB1*05:02:01:01 by one nucleotide substitution at position 351 (G > A) in exon 2.

HLA‐C*15:219 differs from HLA‐C*15:02:01:01 by one nucleotide substitution at position 17 in exon 1.

C*03:489 differs from C*03:02:02:01 by one nucleotide substitution at position 899 in exon 5.

C*14:115 differs from C*14:02:01:01 by one nucleotide substitution at position 1030 in exon 6.

HLA‐DRB3*01:86 differs from HLA‐DRB3*01:01:02:01 by one nucleotide substitution in codon 225 in exon 4.

B*35:460 differs from B*35:03:01:01 by one nucleotide substitution at position 406 in exon 3.

HLA‐A*30:171 differs from HLA‐A*30:01:01:01 by one nucleotide substitution at position 821 in exon 4.

HLA‐B*07:381 differs from B*07:02:01:01 by one nucleotide substitution at position 1046 in exon 7.

A*11:349 differs from A*11:01:01:01 by one nucleotide substitution at position 688 in exon 4.

B*07:384 differs from B*07:02:01:01 by one nucleotide substitution at position 472 in exon 3.

B*07:385 differs from B*07:02:01:01 by one nucleotide substitution at position 660 in exon 4.

A*24:470 differs from A*24:02:01:01 by one nucleotide substitution at position 46 in exon 1.

HLA‐A*02:411 differs from HLA‐A*02:01:01:01 at nucleotides 770 and 771, where Threonine (T) replaces Isoleucine (I) at residue 233.

DQB1*05:235N differs from DQB1*05:03:01:01 by one nucleotide substitution at position 123 in exon 2, resulting in a premature stop codon.

The non‐classical Major Histocompatibility Complex of class II molecules (ncMHCII) HLA‐DM (DM) and HLA‐DO (DO) feature essential functions for the selection of the peptides that are displayed by classical MHCII proteins (MHCII) for CD4+ Th cell surveillance. Thus, although the binding groove of classical MHCII dictates the main features of the peptides displayed, ncMHCII function defines the preferential

HLA‐DQB1*02:01:01:02 differs from HLA‐DQB1*02:01:01:01 by one nucleotide change in intron 2 at position 3949 (G>C).

HLA‐C*08:01:01:05 differs from HLA‐C*08:01:01:02 by one nucleotide deletion (T > −) at position 674 in intron 2.

Some HLA alleles have been shown to be associated with susceptibility to cytomegalovirus (CMV) disease incidence in vitro. The objective of this study was to identify correlations between donor HLA allotypes and CMV disease incidence in patients with acute myeloid leukemia who had undergone allogeneic hematopoietic stem cell transplantation (HSCT). Methods and materials we retrospectively analyzed

Three novel HLA‐A*02:06:01:04 , ‐DRB1*12:02:01:02 , ‐DQB1*03:01:01:07 and five extended HLA‐B*51:01:05 , ‐DRB1*12:02:01:01 , ‐DRB1*14:01:01 , ‐DRB1*14:04:01:01 , ‐DRB1*15:04 alleles.

One nucleotide substitution in codon 304 of HLA‐A*11:01:01:01 results in a novel allele, HLA‐A*11:280.

A novel variant of HLA‐C*03:04:01:47 was identified using Pacific Biosciences SMRT sequencing platform.

HLA‐DQB1*03:222 differs from HLA‐DQB1*03:03:02:01 by a single nucleotide change in exon 3.

HLA‐A*29:128 differs from A*29:02:01:01 by one nucleotide mutation in codon 94.

HLA‐A*31:72 has one nucleotide change from HLA‐A*31:01:02:01 where Histidine (188) is changed to Arginine.

Luminex single antigen flow beads (SAFB) assays are used to monitor anti‐HLA antibodies, which are associated with allograft loss. The primary antibody binding level is evaluated by the mean fluorescence intensity (MFI) provided by the tracing secondary antibody. The aim of this study was to compare the MFI obtained with two secondary antibodies and to evaluate their sensitivity to detect newly developed

The new B*40:462 allele was characterized in a Caucasian Spanish individual.

HLA‐B*52:100 differs from HLA‐B*52:01:01:01 by one nucleotide at position 858 in exon 4.

One nucleotide substitution in codon 39 of HLA‐DRB4*01:01:01:01 results in a novel allele, HLA‐DRB4*01:44.

HLA‐DQB1*05:02:23 differs from DQB1*05:02:01 by a mutation at nucleotide 450.

We have developed a protocol regarding the genomic characterization of the MICA gene by NGS. The amplicon includes the full length of the gene and is about 13 kb. A total of 156 samples were included in the study. Ninety‐seven of these samples were previously characterized at MICA by legacy methods (Sanger or SSO) and were used to evaluate the accuracy, precision, specificity, and sensitivity of the

DPB1 and DPA1 genes share the same promoter region. Single‐nucleotide polymorphisms (SNPs) within the regulatory regions of DP have been reported. This study hypothesizes that by including the SNPs in the promoter region of DP, extended haplotypes are defined, and promoter polymorphism is more extensive than what is currently reported. To identify the SNPs in the region of interest, the DP region spanning

PCR‐sequence‐specific oligonucleotide (PCR‐SSO) is commonly used for HLA‐typing. We recently replaced LabType SSO HD kit for HLA‐C typing with the XR kit (OneLambda, Inc.). We used 137 patients' samples representing unique most likely HLA‐C allele combinations to compare these kits' performance. The XR kit decreased the number of allele ambiguities with a median of 26.1% (first to third quartiles 20%

A*11:334 differs from A*11:01:01 by one nucleotide change at nucleotide 446 in exon 3 from C to T.

A single nucleotide change (C to T) in HLA‐DQB1*01:03:01:03 results in the novel allele, HLA‐DPA1*01:03:01:21.

One nucleotide change (G > C) in the exon 4 of HLA‐C*07:02:01:01 results in the novel allele, HLA‐C*07:862.

Characterization of three novel HLA‐DQB1*05 variants, HLA‐DQB1*05:01:01:08 , ‐DQB1*05:02:01:07 and ‐DQB1*05:03:01:05 .

Surface expression of human leukocyte antigen (HLA)‐class I molecules is critical for modulating T/natural killer lymphocytes' effector functions. Among HLA molecules, HLA‐C, the most recently evolved form of class I antigens, is subjected to both transcriptional and multiple post‐transcriptional regulation mechanisms affecting its cell surface expression. Among the latter a region placed in the 3′

Human Leucocyte antigen‐C (HLA‐C) is a classical HLA class I molecule that binds and presents peptides to cytotoxic T lymphocytes in the cell surface. HLA‐C has a dual function since it also interacts with KIR receptors expressed in NK and T cells, modulating their activity. The structure and diversity of the HLA‐C regulatory regions, as well as the relationship among variants along the HLA‐C locus

Characterization of five novel HLA‐DQA1*01 variants, HLA‐DQA1*01:01:01:08, −DQA1*01:02:01:14, −DQA1*01:02:02:05, −DQA1*01:03:01:10 and −DQA1*01:05:01:03.

Accurate rapid genotyping of the genes within the HLA region presents many difficulties because of the complexity of this region. Here we present the results of our proof of concept nanopore‐based long read polymerase chain reaction (PCR) solution for HLA genotyping. For 15 HLA anthropology‐based samples and 13 NHS Blood and Transplant derived samples 40 ng of genomic DNA underwent long‐range PCR for

Anti‐“Mia” is the most frequent irregular RBC antibody in Taiwan due to high prevalence of Miltenberger antigens. Dialysis patients, a special patient group that needs frequent transfusions of RBCs, may have the greatest risk for developing anti‐“Mia” antibodies. The aim of this study was to investigate the association between specific HLA‐DRB1 alleles and Mi alloimmunization among dialysis patients

COVID‐19 is a respiratory disease caused by a novel coronavirus and is currently a global pandemic. HLA variation is associated with COVID‐19 because HLA plays a pivotal role in the immune response to pathogens. Here, 82 individuals with COVID‐19 were genotyped for HLA‐A, ‐B, ‐C, ‐DRB1, ‐DRB3/4/5, ‐DQA1, ‐DQB1, ‐DPA1, and ‐DPB1 loci using next‐generation sequencing (NGS). Frequencies of the HLA‐C*07:29

Pigs are especially useful large animal models, however, limited availability of commercially available antibodies for immunoblotting presents a significant obstacle facing preclinical xenotransplantation research. Major histocompatibility complex class I (MHC‐I) molecule expression enhancement by nucleotide‐binding oligomerization domain (NOD)‐like receptor family with a caspase recruitment domain

Four new HLA alleles characterized by NGS, B*40:455 , C*03:521 , C*03:04:81 and DQB1*03:431 .

HLA‐DQA1*01:49 differs from HLA‐DQA1*01:01:01:06 by one nucleotide substitution in codon 9 in exon 2.

HLA‐DQA1*03:01:06 differs from HLA‐DQA1*03:01:01:01 by one nucleotide substitution in codon 9 in exon 2.

HLA‐DQA1*03:15 differs from HLA‐DQA1*03:01:01:01 by one nucleotide substitution in codon 79 in exon 2.

HLA‐DPB1*1089:01 differs from HLA‐DPB1*02:01:02:04 by two nucleotide substitutions in codon 43 in exon 2.

HLA‐DPB1*1098:01N differs from HLA‐DPB1*03:01:01:01 by one nucleotide substitution in codon 128 in exon 3.

In [1], the authors re‐analyzed the sequences of the two samples described in this publication and observed that the novel allele HLA‐C*03:04:01:38 was identified in only one individual, ID‐149P. The second individual, ID‐205C mentioned in report, had an additional sequence variation, which was later submitted to WHO Nomenclature Committee for Factors of the HLA System and was assigned as HLA‐C*03:04:01:41