HLA-C*01:224N, a novel null HLA-C allele characterized by two next-generation sequencing methods.

We describe here the novel HLA-C*01:224N allele which has a premature stop codon in exon 3.

Characterization of the novel HLA-DRB1*11:296 allele by two next-generation sequencing methods.

The novel HLA-DRB1*11:296 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-C*06:346 allele by two next-generation sequencing methods.

The novel HLA-C*06:346 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-A*01:406 allele by two next generation sequencing methods.

The novel HLA-A*01:406 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-A*01:405 allele by two next generation sequencing methods.

The novel HLA-A*01:405 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-DRB1*04:334 allele by two next-generation sequencing methods.

The novel HLA-DRB1*04:334 allele was characterized using two next-generation sequencing technologies.

Characterization of the novel HLA-A*23:118 allele by two next-generation sequencing methods.

The novel HLA-A*23:118 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-C*07:01:105 allele by two next-generation sequencing methods.

The novel HLA-C*07:01:105 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-B*40:02:35 allele by two next-generation sequencing methods.

The novel HLA-B*40:02:35 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-B*15:10:08 allele by two next-generation sequencing methods.

The novel HLA-B*15:10:08 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-C*02:207 allele by two next-generation sequencing methods.

The novel HLA-C*02:207 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-A*03:425 allele by two next-generation sequencing methods.

The novel HLA-A*03:425 allele was characterized using two next-generation sequencing technologies.

Characterization of the novel HLA-C*05:01:68 allele by two next-generation sequencing methods.

The novel HLA-C*05:01:68 allele was characterized using two next generation sequencing technologies.

Characterization of the novel HLA-C*07:977 allele by two next-generation sequencing methods.

The novel HLA-C*07:977 allele was characterized using two next generation sequencing technologies.

HLA-B*48:53, a novel HLA-B allele with two exonic mutations.

The novel HLA-B*48:53 allele was characterized using two next generation sequencing technologies.

Easy-HLA: a validated web application suite to reveal the full details of HLA typing.

Motivation: The HLA system plays a pivotal role in both clinical applications and immunology research. Typing HLA genes in patient and donor is indeed required in hematopoietic stem cell and solid-organ transplantation, and the histocompatibility complex region exhibits countless genetic associations with immune-related pathologies. Since the discovery of HLA antigens, the HLA system nomenclature and typing methods have constantly evolved, which leads to difficulties in using data generated with older methodologies.

HCMV triggers frequent and persistent UL40-specific unconventional HLA-E-restricted CD8 T-cell responses with potential autologous and allogeneic peptide recognition.

Immune response against human cytomegalovirus (HCMV) includes a set of persistent cytotoxic NK and CD8 T cells devoted to eliminate infected cells and to prevent reactivation. CD8 T cells against HCMV antigens (pp65, IE1) presented by HLA class-I molecules are well characterized and they associate with efficient virus control. HLA-E-restricted CD8 T cells targeting HCMV UL40 signal peptides (HLA-EUL40) have recently emerged as a non-conventional T-cell response also observed in some hosts.

Polymorphism in programmed cell death 1 gene is strongly associated with lung and kidney allograft survival in recipients from CMV-positive donors.

Background: Cytomegalovirus (CMV) has a role in chronic rejection and graft loss in kidney transplant (KTx) and lung transplant (LTx) recipients. In addition, donor CMV seropositivity is an independent risk factor for renal graft loss. The anti-CMV response might modulate this risk.

MICA Mutant A5.1 Influences BK Polyomavirus Reactivation and Associated Nephropathy After Kidney Transplantation.

Background: BK polyomavirus (BKPyV) frequently reactivates in kidney transplant recipients during immunosuppressive therapy and triggers BKPyV-associated nephropathy and graft rejection. Determining effective risk factors for BKPyV reactivation is required to achieve efficient prevention.

Methods: This study investigated the role of major histocompatibility complex (MHC) class I-related chain A (MICA) in BKPyV reactivation in a cohort of 144 transplant donor/recipient pairs, including recipients with no reactivation (controllers) and those with mild (virurics) or severe (viremics) BKPyV reactivation after graft receipt.

MICA variant promotes allosensitization after kidney transplantation.

MHC class I-related chain A (MICA) antigens are surface glycoproteins strongly implicated in innate immunity, and the MICA gene is highly polymorphic. Clinical observations suggest a role for donor MICA antigens expressed on transplant endothelial cells in the alloimmune response, but the effect of MICA genotype is not well understood. Here, we investigated the immunologic effect of the A5.

Both the nature of KIR3DL1 alleles and the KIR3DL1/S1 allele combination affect the KIR3DL1 NK-cell repertoire in the French population.

NK-cell functions are regulated by many activating and inhibitory receptors including KIR3DL1. Extensive allelic polymorphism and variability in expression can directly alter NK-cell phenotype and functions. Here we investigated the KIR3DL1(+) NK-cell repertoire, taking into account the allelic KIR3DL1/S1 polymorphism, KIR3DL1 phenotype, and function.

Investigation of the impact of HLA-DPB1 matching status in 10/10 HLA matched unrelated hematopoietic stem cell transplantation: results of a French single center study.

The impact of HLA-DPB1 mismatches after unrelated hematopoietic stem cell transplantation (HSCT) remains controversial. We retrospectively analyzed the impact of permissive/non-permissive HLA-DPB1 mismatches on the outcome of 141 patients who underwent 10/10 HLA allelic-matched unrelated HSCT. Each pair was classified according to the 3 (TCE3) and 4-group (TCE4) algorithm based on DPB1 alleles immunogenicity.

Identification of a gene expression profile associated with operational tolerance among a selected group of stable kidney transplant patients.

Despite their utility, immunosuppressive treatments have numerous side effects, including infectious complications, malignancies and metabolic disorders, all of which contribute to long-term graft loss. In addition to the development of new pharmaceutical products with reduced toxicity and more comfortable modes of administration, tailoring immunosuppression according to the immune status of each patient would represent a significant breakthrough. Gene expression profiling has been shown to be a clinically relevant monitoring tool.

Granulocyte antibody screening: evaluation of a bead-based assay in comparison with classical methods.

Background: Granulocyte antibodies have been implicated in allo- and autoimmune neutropenia and in transfusion reactions.

Study Design And Methods: Fifty-one sera from suspected alloimmune neutropenia or transfusion-related acute lung injury (TRALI) and 40 sera from suspected autoimmune neutropenia were tested for granulocyte antibodies using LABScreen MULTI (One Lambda, Inc.), compared with classical tests (flow cytometry [FC] and granulocyte agglutination [GAT] followed by monoclonal antibody-specific immobilization of granulocyte antigens [MAIGA]).