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HLA-A*11:423 differs from HLA-A*11:01:01:01 by a non-synonymous nucleotide substitution in codon 170, changing Arginine to Lysine. This article is protected by copyright. All rights reserved.

HLA-C*06:325 differs from HLA-C*06:02:01:01 by a non-synonymous nucleotide substitution in codon 145, changing Arginine to Histidine.

Introduction Chimerism is defined as coexistence of different cell lines in an individual. 46,XX/46,XY chimerism is very rare and exhibits broad range of clinical phenotypes. Most cases are detected at infancy or younger age due to disorders of sex development, while phenotypically normal cases are incidentally discovered through abnormal blood grouping results or multiple genotypes in HLA. Objective Aim was to determine the genetic expression of numerous HLA alleles detected in phenotypically normal 46,XX/46,XY chimerism. Materials and methods A patient was admitted for lung transplantation due to end-stage pulmonary disease. Pre-transplantation work-up included blood group typing and HLA DNA typing analyses. Peripheral blood and hair follicle specimens were used to confirm unusual tri-allelic results by high-resolution PCR-SBT. Cytogenetic analyses of karyotyping, FISH and chromosomal microarray were done. Flowcytometry crossmatch analysis was conducted using lymphocytes and anti-HLA sera defined by Luminex panel reactive antibody test (One Lambda, Inc., Canoga Park, CA), to determine antigen expression of HLA alleles. Results 46,XX/46,XY chimerism was confirmed through series of cytogenetic analyses. HLA typing of the patient revealed three alleles from HLA-A, -B and -DRB1 loci. Antigen expression of all 3 HLA alleles was confirmed by flow cytometry crossmatch. Discussion A case of normal phenotype 46,XX/46,XY chimerism was detected for the first time in Korean patient admitted for lung transplantation. Cytogenetic results were confirmatory for chimerism and HLA typing using PCR-SBT method was able to detect the presence of 3 HLA alleles. Flowcytometry crossmatch was proven sensitive for detecting antigen expression of different cell lines of small proportions.

The novel HLA-C*03:539 allele differs from HLA-C*03:04:01:01 by one nucleotide substitution at codon 26.

The HLA-DPA1*02:02:08 allele differs from HLA-DPA1*02:02:02:01 by a synonymous nucleotide substitution at codon 194.

HLA-DQB1*03:457 differs from HLA-DQB1*03:02:01:01 by a non-synonymous nucleotide substitution in codon 95, changing valine to glutamic acid.

Introduction ABO-incompatible transplantation has expanded the limited donor pool for kidney transplantation. Despite the successful desensitization protocols and immunosuppression, undesirable cases of hyperacute rejection occurs. Objective Flow cytometry was used to measure isoagglutinin titer and its IgG subclasses in assessment of the cause of hyperacute rejection in ABO-incompatible kidney transplantation. Materials and methods The recipient was admitted for kidney transplantation due to end-stage renal disease. Pre-transplantation work-up for ABO-incompatible kidney transplantation included blood group typing, HLA DNA typing and HLA antibody analyses. HLA crossmatch analysis was conducted using donor lymphocytes and anti-HLA antibody assay using Luminex panel reactive antibody test (One Lambda, Inc., Canoga Park, CA). Desensitization protocol was composed of therapeutic plasma exchange sessions and rituximab. Results Despite negative HLA crossmatch results, a case of hyperacute rejection occurred after living donor kidney transplantation. Rejection resulted in immediate removal of graft, and the patient later received a second kidney transplantation. Retrospective evaluation of isoagglutinin titer and its subclasses using flow cytometry identified the cause of rejection to increased IgG1 subclass. Desensitization protocol for ABO-incompatible kidney transplantation now implements further caution for blood group O recipients. Discussion Hyperacute rejection resulting from increased IgG1 isoagglutinin subclass has not been previously confirmed using flow cytometry. Unfortunate outcome of this rejection case provides insight to how we should approach and ensure successful ABO-incompatible kidney transplantation.

Three novel HLA alleles, HLA-A*26:118, DQB1*02:65 and DPB1*05:01:07, were identified and confirmed by monoallelic sequencing.

The novel HLA-B*27:198 allele differs from HLA-B*27:05:02:01 by one nucleotide substitution at codon 45.

Four novel HLA alleles identified in Korean individuals and confirmed by monoallelic sequencing.

Aim Allele level interpretation of HLA DR-3/4/5 is encouraged as low-expression loci mismatch can affect the outcome of organ transplantation. Here we assess the HLA-DRB3/4/5 allele frequency in Korean population and report the occurrence rate of post-transplantation HLA-DR donor specific antigen (DSA) according to eplet mismatches including HLA-DRB1 and HLA-DRB3/4/5. Methods High resolution genotyping of HLA-DRB3/4/5 at 6-digit level was done using blood samples from 150 unrelated healthy Koreans. Regarding assessment of the effect on organ transplantation, there were 272 patients with pre- and post-op panel reactive antibody (PRA) results during September 1st, 2012 and August 31th, 2017. Their post-transplantation de novo DSA occurence was analyzed by HLA-DR eplet mismatches of HLA-DRB1 and HLA-DR3/4/5. Results Four HLA-DRB3 alleles, three HLA-DRB4 alleles and three HLA-DRB5 alleles were found at 6-digit level (Table). Total 32 HLA-DRB1-DRB3/4/5 haplotype combinations were found (data not shown). The number of eplet mismatch with no post-transplantation de novo DSA was seven for HLA-DR and cumulative DSA frequency was observed up to 9.8% (Image). Conclusions HLA-DRB3/4/5 allele frequency and HLA-DRB1-DRB3/4/5 haplotype frequency were analyzed at 6-digit level for the first time in Koreans. Our result demonstrates that degree of HLA-DR eplet mismatches of all HLA-DR loci could affect generation of post-op de novo DSA. These results will be useful for PRA interpretation and understanding the impact of low-expression loci on organ transplantation.

The new allele, A*11:251N, differs from A*11:01:01 by insertion of two nucleotides at position 204-205.

The new allele HLA-C*03:03:35 showed one nucleotide difference with C*03:03:01:01 at position 408 (G>T).

HLA-DQB1*04:01:05 differs from DQB1*04:01:01 by a single nucleotide substitution at codon 30 (TAC>TAT).

Background A dysregulated mucosal immune response to the intestinal environment in a genetically susceptible host is hypothesized to be critical to the pathogenesis of Crohn's disease (CD). Therefore, we examined CD-susceptibility genes involved in the immune response through a genome-wide association study and consecutive genotyping of human leukocyte antigens (HLAs) and killer cell immunoglobulin-like receptors. Methods An initial genome-wide association study was performed with 275 CD patients and 2369 controls from a Korean population. To validate the loci identified in the genome-wide association study, replication genotyping was performed in a different cohort of 242 CD patients and 1066 controls. Finally, high-resolution genotyping of HLA and killer cell immunoglobulin-like receptor was performed. Results Four susceptibility loci, a promoter region in tumor necrosis factor (ligand) superfamily member (TNFSF15) and 3 independent regions in HLAs, showed significant associations with CD. Among them, rs114985235 in the intergenic region between HLA-B and HLA-C showed the strongest association, with an increased risk of CD (P = 8.71 × 10; odds ratio, 2.25). HLA typing in this region showed HLA-C*01 to be responsible for the association of CD among 43 HLA-B and HLA-C genotypes identified in the Korean population. However, the interaction of HLA-C with killer cell immunoglobulin-like receptor had little effect on the development of CD. Conclusions We newly identified HLA-C*01 as a prominent CD-susceptibility HLA allotype in the Korean population. In addition, these results confirm that genetic variations in immune response genes, such as HLAs and TNFSF15, are important host factors for the pathogenesis of CD.

Human leukocyte antigens (HLAs) are useful markers for anthropological investigations because the allele and haplotype distributions at these loci vary widely among ethnic groups. HLA frequencies in Koreans, however, have not previously been analyzed on a phylogenetic basis. We determined the allele frequencies of four HLA class II (HLA-DRB1, -DQA1, -DQB1, and -DPB1) loci in 149 unrelated Korean individuals using a sequence-based typing method. A total of 29 HLA-DRB1, 17 HLA-DQA1, 16 HLA-DQB1, and 15 HLA-DPB1 alleles were identified. The most common allele at each locus was DRB1*0901, DQA1*0102, DQB1*0301, and DPB1*0501, respectively. Four-locus allelic association analysis showed the existence of 25 DRB1-DQA1-DQB1-DPB1 haplotypes with a frequency greater than 0.010. A dataset comprising ethnicity-specific information from published literature and the dbMHC database, as well as the allele frequencies determined in this study, was subjected to phylogenetic analysis. The analysis showed that Koreans are most closely related to Japanese and Han Chinese from Shandong province. Correspondence analyses showed that the current Korean population is located in a position intermediate between the northern and southern East Asian groups, supporting the theory of a bi- and/or multidirectional route of migration of early Korean settlers. This report can be used for anthropological studies, and may also be of use in the International Hematopoietic Stem Cell Sharing program.

Major histocompatibility complex (MHC) class I chain-related gene A (MICA) is located within the human MHC, centromeric to HLA-B and telomeric to HLA-DRB1. The location of MICA in the MHC indicates the presence of linkage disequilibrium with human leukocyte antigen (HLA). Like HLA, MICA is highly polymorphic; however, the information available for MICA polymorphisms is not as comprehensive as that for HLA polymorphisms. We estimated the allelic frequencies of MICA and haplotypes with HLA-B and HLA-DRB1 at high-resolution in a population of 139 unrelated Korean individuals by applying the newly developed method of sequence-based typing (SBT). A total of 17 MICA alleles were identified. The most frequent allele was MICA*010 (19.4%), followed by alleles *00201 (17.6%), *00801 (14.7%), *01201 (9.4%), *004 (8.3%) and *049 (7.9%). The most common two- and three-locus haplotypes were HLA-B*1501-MICA*010 (10.4%), MICA*010-HLA-DRB1*0406 (5.8%) and HLA-B*1501-MICA*010-HLA-DRB1*0406 (5.8%). This is the first study to provide such high-resolution information on the distribution of haplotypes comprising MICA, HLA-B and HLA-DRB1 in Korean individuals, a level of resolution made possible by use of the SBT method. The results of this study should help determine the mechanisms underlying diseases associated with MICA polymorphisms in Korean individuals.

Background: There has been no study for evaluating the associations of human leukocyte antigen (HLA) class I and II alleles with toluene diisocyanate (TDI)induced asthma in an Asian population. Objective: The aim of this study was to investigate a susceptible or protective marker of HLA class I and II alleles in TDI-induced asthma. Methods: Fifty-five patients with TDI-induced asthma patients (group I) showing positive responses on TDI bronchoprovocation test, 47 asymptomatic exposed subjects (group II) and 95 unexposed healthy nonatopic controls (group III) were enrolled in our study. HLA class I and II genotyping was done by the direct DNA sequencing method. Results: The allelic frequency of C*09 (15.5%) was significantly higher in group I than in group III (6.8%, P ¼ 0.019), but this statistical significance disappeared after correction was made for multiple comparisons. On two-locus and threelocus haplotype analysis, the allelic frequency of HLA DRB1*15-DPB1*05 in group I (10.6%) was significantly higher than that of group II (0%, P ¼ 0.001) and group III (2.5%, P ¼ 0.003). The allelic frequencies of HLA A*02DRB1*15, A*02-DQB1*06, B*62-C*09 and A*02-DRB1*15-DQB1*06 were significantly higher in group I (8.5%, 10.3%, 8.2% and 6.8%, respectively) than those allelic frequencies of group III (1.3%, P ¼ 0.002; 1.6%, P ¼ 0.001; 0.6%, P < 0.0001; 0%, P < 0.0001, respectively). The allelic frequencies of HLA DQB1*06-DPB1*05 and DRB1*15-DQB1*06-DPB1*05 were significantly higher in group I (16.0% and 10.5%) than those in group II (2.5%, P ¼ 0.001; 0%, P ¼ 0.001), while the frequencies of DRB1*09-DPB1*05 and DRB1*09DQB1*0303-DPB1*05 were significantly lower in group I (0% and 0%) than those of group II (7.4%, P ¼ 0.004; 7.5%, P ¼ 0.004). These differences remained statistically significant even after the correction for multiple comparisons. Conclusions: The HLA haplotype DRB1*15-DPB1*05 can be a susceptibility gene marker for the development of TDI-induced asthma among the exposed workers in the Korean population.

Background Vascular endothelial growth factor (VEGF) has been suggested to be a key mediator in the development of atopy and T H 2 inflammation. Objective We sought to evaluate the effects of variations in the gene coding VEGF receptor (VEGFR) 2 on intermediate phenotypes of asthma in the Korean population. Methods A cohort of 2055 children and adolescents responded to a questionnaire concerning asthma symptoms and risk factors and underwent methacholine bronchial challenge and skin tests. The VEGFR2 gene, including the promoter area, was sequenced on 24 healthy subjects to discover informative single nucleotide polymorphisms (SNPs; minor allele frequency >2%). After haplotype reconstruction, 4 tagging SNPs (IVS6+54A>G, +889G>A, +1416T>A, and IVS25-92G>A) were scored. These SNPs were also scored in 480 adult asthmatic patients to verify the above genetic association study. Results The prevalence of atopy was associated with a single SNP (+889G>A) of VEGFR2 with borderline significance ( P = .048; relative risk, 1.13; 95% CI, 1.00-1.28). However, haplotype analysis showed that the atopy prevalence was strongly associated with a haplotype (AGAG) of VEGFR2 ( P = .002; relative risk, 1.25; 95% CI, 1.09-1.42). As for airway hyperresponsiveness, neither individual SNPs nor haplotypes were found to be associated. Interestingly, the significant association was also found between atopy and the AGAG haplotype among adult asthmatic patients ( P = .008; odds ratio, 1.66; 95% CI, 1.14-2.44). Conclusions The present study demonstrated that genetic variations of VEGFR2 are significantly associated with atopy in the Korean population.

Background and Objective Human leukocyte antigen (HLA) class II gene products are involved in the antigen presentation of exogenous antigens. The aim of this study was to evaluate whether specific immunoglobulin (Ig)E responses to purified major allergens of Dermatophagoides pteronyssinus (Der p 1 and Der p 2) were associated with genotypes of HLA-DRB1 alleles. Subjects and Methods Peripheral venous blood samples were collected from two groups of unrelated Korean adolescents: 168 subjects with positive skin response (wheal ≥3 mm) to crude D. pteronyssinus allergens and 94 age-matched controls with negative skin response and low serum-specific IgE to crude D. pteronyssinus allergens. The former group was found to contain 104 with high serum-specific IgE to crude D. pteronyssinus allergens, 100 with high serum-specific IgE to Der p 1, and 122 with high serum-specific IgE to Der p 2. Genotypes of the HLA-DRB1 alleles were determined using polymerase chain reaction-sequence specific oligonucleotide probes. Results HLA-DRB1*07 was significantly higher in subjects with a high serum-specific IgE response to crude D. pteronyssinus allergens than the controls (16.3% vs 3.2%, odds ratio [OR] = 5.93, corrected P [ Pc ] = 0.02). The excess of DRB1*07 was more marked in those with high serum-specific IgE responses to Der p 1 or Der p 2 than the controls (20.0% vs 3.2%, OR=7.58, Pc = 0.004; 18.9% vs 3.2%, OR=7.05, Pc = 0.006). Among subjects with high serum IgE to Der p 1, DRB1*13 significantly increased than the controls (32.0% vs 13.8%, OR=2.93, Pc = 0.03). Conclusions We clearly observed the association between HLA-DRB1 alleles and specific IgE responsiveness to D. pteronyssinus major allergens. The molecular mechanism of HLA-DRB1*07 and DRB1*13 involvement in D. pteronyssinus -specific IgE responsiveness awaits further investigation.

The new allele DQB1*05:06 showed one nucleotide difference with DQB1*05:03:01 at codon 40 (TTC/TTG).

New allele B*4617 showed one nucleotide difference with B*460101 at codon 167 (TGG--TCG).

Because Korean society is fast becoming multi-ethnic, the determination of ambiguous human leukocyte antigen (HLA) types using HLA allele frequencies is becoming less applicable. In this study, we focused on the development of new technical methods to directly resolve the ambiguities arising from HLA genotyping. One hundred and fifty unrelated healthy Korean adults were included in this study. All alleles from each HLA locus were first divided into 2-4 groups, with each group amplified in a single PCR tube (multi-group-specific amplification, MGSA). To resolve phase ambiguities, some allele groups were also amplified separately in small group-specific amplification (SGSA) tubes. In order to then resolve incomplete sequence ambiguities, primers for MGSA and SGSA were initially designed to cover additional exons. If needed, a heterozygous ambiguity resolving primer (HARP) or sequence specific primer (SSP) was also used. When MGSA and SGSA methods were applied, the rate of phase ambiguity was greatly reduced to an average of 6% (1.3% in HLA-A, 15.7% in -B, and 2.0% in -C). Additional HARP and SSP methods could resolve all the phase ambiguities. Using our proposed method, we also detected three alleles that have not been previously reported in Korea, C*04:82, C*07:18, and C*08:22, and report 6-digit level HLA allele and haplotype frequencies among Koreans. In conclusion, the use of MGSA/SGSA for the initial amplification step is a cost-effective method facilitating timely and accurate reporting, given the continuing increase in the ethnic diversity of the Korean population. The MGSA described here can be applicable to various populations and thus could be shared by the majority of HLA typing laboratories. However, efforts to solve HLA ambiguity should continue, because SGSA, HARPs and SSPs would be specific to a particular population.

The new allele, DRB1*04:10:03, showed one nucleotide difference with DRB1*04:10:01 (705C>T).

Major histocompatibility complex (MHC) class I chain-related gene B (MICB) is located within the human MHC class I region. The location of MICB in the MHC region may imply the presence of linkage disequilibrium with polymorphic MICA and human leukocyte antigen (HLA) loci. MICB is also polymorphic; however, MICB polymorphisms have not been investigated in Koreans. Using sequence-based typing (SBT), we estimated the allelic frequencies of MICB and haplotypes with MICA, HLA-B, and HLA-DRB1 at high resolution in a population of 139 unrelated Korean individuals. Eight MICB alleles were identified. The most frequent allele was MICB*005:02/*010 (57.2%), followed by *002 (11.5%), *004 (8.3%), *005:03 (8.3%), and *008 (6.8%). The most common two-locus haplotypes were MICB*005:02/*010-MICA*010 (19.4%), MICB*005:02/*010-DRB1*15:01 (6.5%), and MICB*005:02/*010-B*15:01 (10.4%); the most common three-locus haplotypes were B*15:01-MICA*010-MICB*005:02/*010 (5.8%) and MICA*010-MICB*005:02/*010-DRB1*04:06 (10.4%); and the most common four-locus haplotype was B*15:01-MICA*010-MICB*005:02/*010-DRB1*04:06 (5.8%). This is the first study to provide information about MICB allele frequencies and haplotypes with HLA in Koreans. These study results should help understand mechanisms of disease association between the MICB locus and neighboring loci in Koreans.

The new allele B*40:155N showed five nucleotide insertion between nucleotide 594 and 595 (codon 174 and 175) compared to B*40:01:01.

The new allele DRB1*13:99 showed one nucleotide difference with DRB1*13:02:01 at codon 51 (ACG/AAG).

We encountered a case that exhibited a discrepancy in human leukocyte antigen-A (HLA-A) type determined by sequence-based typing (SBT) and sequence-specific primer (SSP) molecular typing. The child of this case was identified as A* 02:01 homozygote and A* 02, A* 24, respectively. The HLA-A type of his father was A* 02:01, 26:01, but low-resolution SSP also showed unexpected amplification with A* 24 primers as with the child. Serologic typing of the child and the father was A2/blank and A2/A26, respectively. Sequencing analysis of the A* 24 variant in the child and the father showed a complete deletion of all introns of the A* 24:02 allele. Though rare, this type of processed pseudogene variant can be one of the causes of discrepancies between high- and low-resolution HLA typing.

The new allele B*40:02:18 showed one nucleotide difference with B*40:02:01 at codon 111 (CGC/CGT).

The new allele A*11:01:54 shows one nucleotide difference from A*11:01:01 at codon 35 (CGG/AGG).

The new allele A*11:164 showed one nucleotide difference with A*11:01:01 at codon 151 (CAT>CCT).

The new allele B*39:60 showed one nucleotide difference with B*39:01:01 at codon 152 (GTG/GCG).

This study was performed to assess the probability of finding HLA-matched donors for Korean and Japanese patients from unrelated marrow donor registries of both countries. A simulation study of donor search was carried out using the donor pools of the Korean Marrow Donor Program (KMDP) with 10,244 and the Japan Marrow Donor Program (JMDP) with 53,411 HLA-A, -B, -DR typed donors. The records of a total of 184 actual Korean patients and 1,302 simulated Japanese patients were searched and A, B, DR-matched donors were found for 28% of Korean and 76% of Japanese patients from the KMDP and JMDP pools, respectively. Of those patients who could not find matched donors in the registry of their own country, 30% of Koreans could find matched donors in the JMDP and 10% of Japanese in the KMDP pools. It can be concluded that future international collaboration between Korea and Japan would be very effective for unrelated bone marrow transplantations.

Microarray technology makes high-throughput genotyping possible by permitting the simultaneous analysis of large sets of genes on a small reaction slide. Human leukocyte antigen (HLA) loci showing high polymorphisms are suitable targets for microarray. In this study, we developed a microarray kit with newly designed oligonucleotide probes for the genotyping of HLA-A and -DRB1. In total, 42 probes were designed to hybridize to polymorphic sites for HLA-A and 36 for HLA-DRB1. Asymmetric polymerase chain reaction (PCR) using four primers was performed to amplify exon 2 of HLA-DRB1, whereas symmetric PCR was performed to amplify both exons 2 and 3 of HLA-A. Evaluation of performance using samples from 138 Koreans disclosed consistent microarray results with all sequence-based typing at the low-resolution level. Despite the occurrence of ambiguities in 35 HLA-A (25.4%) and 5 HLA-DRB1 (3.6%) cases, correct genotypes were assigned with high certainty by referring to allele distribution in Koreans. These data clearly indicate that our newly developed microarray kit is optimal in determining correct genotypes at the low-resolution level in Koreans.

New allele Cw*033802 showed one nucleotide difference with Cw*0338 at codon 99 (TAC-->TAT).

The new allele DQB1*05:50 showed one nucleotide difference with DQB1*05:03:01:01 at codon 39 (CGC/CAC).

In this report, we describe the identification of a human leucocyte antigen-A*11 (HLA-A*11) nucleotide sequence variant, a new HLA-A*1120 by using sequence-based typing (SBT). The new allele was detected during routine HLA typing by high-resolution SBT. Allele A*1120 showed one nucleotide difference with A*110101 at codon 152 (GCG-->GAG) resulting in an amino acid change from alanine to glutamate. Residue 152 is located on alpha(2)-helix of HLA class I molecule and involved in peptide binding by constructing E pocket of peptide-binding groove, implying that the change of the residue 152 would affect the binding affinity of peptides to A*1120 allele.

In this report, we describe the identification of an HLA-A*31 nucleotide sequence variant, a new HLA-A*3111, in three members of a Korean family by using sequence-based typing (SBT). The new allele was detected during routine HLA typing by high-resolution SBT. Allele A*3111 showed one nucleotide difference with A*310102 at codon 165 (GTG--CTG) resulting in an amino acid change from valine to leucine (V165L). Serologic reactivity was shorter than normally expected.

The sequence of the C*03:02:02:03 differs from that of C*03:02:02:01 by one nucleotide substitution in the 5' UTR at position -57 (C>A).

Background: The reports from in vitro studies that β 2 -adre-nergic receptor (B2AR) polymorphisms are associated with agonist-promoted downregulation have evoked considerable research interest for the roles of these polymorphisms to the pathogenesis of asthma. Objective: We sought to evaluate the association between asthma phenotypes and B2AR polymorphisms at 2 sites (Arg16 → Gly16 and Gln27 → Glu27) in the general population. Methods: Four hundred forty unrelated Korean adults were randomly selected, and asthma phenotypes were determined with a questionnaire, immunoassay, skin prick testing, and methacholine bronchial provocation testing. Genotypes of B2AR polymorphisms were determined with PCR-based methods. Results: No significant association was found between B2AR alleles and haplotypes and total IgE levels, skin test responses to aeroallergens, and bronchial responsiveness to methacholine. Among the atopic subjects, however, numbers of both Arg16 alleles and Arg16-Gln27 haplotypes were negatively associated with nocturnal cough, and in contrast, Gly16-Gln27 was positively associated with it. Conclusion: B2AR polymorphisms may play an important role in the expression of nocturnal cough in atopic subjects but not in the expression of atopy and bronchial hyperresponsiveness in a general population. (J Allergy Clin Immunol 2002;109:630-5.)

The new allele C*03:93 showed one nucleotide difference with C*03:04:01 at codon 140 (GCT/ACT).

The DRB1*11:95 showed a single nucleotide difference with the DRB1*11:01:01 allele at codon 10 (TAC/TGC).

In this report, we describe the identification of an human leucocyte antigen-Cw*0102 (HLA-Cw*0102) nucleotide sequence variant, a new HLA-Cw*010203, in a case - control study by using sequence-based typing. Allele HLA-Cw*010203 showed one nucleotide difference with HLA-Cw*010201 by a silent substitution at codon 130 (CTG-->CTA).