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Results for “HLA-DR Antigens”

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At least 19 recordsLinked to original sources
PubMed1978

Reactivity of a rabbit antiserum against highly purified HLA-DR antigens.

A rabbit antiserum has been raised against highly purified, detergent-solubilized HLA-DR antigens. Externally or internally labelled surface glycoproteins from B-lymphocytes, epidermis, macrophages, and B-lymphoma cell lines reacted with the antiserum which precipitated polypeptide chains with the molecular weights 28,000 and 34,000. Such polypeptide chains were not observed when the antiserum was reacted with T-lymphocytes, T-cell lymphoma lines, kidney, brain, thymus and spermatozoa. Fab-fragments of the antiserum completely abolished the cytotoxic action of HLA-DR allantisera but had no effect on the cytotoxicity mediated by HLA-A,B and C loci antisera. Moreover, the rabbit antiserum reacted with the same molecules as the HLA-DR alloantisera. Fab-fragments of the rabbit antiserum completely abolished the MLR response and from the kinetics of the inhibition it is concluded that the Fab-fragments may interfere primarily with the initial recognition phase of the MLR.

Animals↗
PubMed1978

Matching for B-cell antigens of the HLA-DR series in cadaver renal transplantation.

Stored and fresh lymphocytes from 84 donors and recipients of cadaveric renal allografts have been retrospectively typed for 7 HLA-DR antigens. The match between donor and recipient was graded as 2, 1, or 0 identities. Graft function was assessed by (i) failure or success at 3 months, (ii) serum-creatinine at 3 and 6 months, and (iii) the number of rejection episodes occurring within 3 months. All 4 recipients with 2 identities had good 3-month function, and all are still functioning at 5--19 months. Recipients with 1 identity had both a higher success-rate and better quality of function than those with 0 identities. Although the differences do not reach significance, a continuing prospective study of HLA-DR matching is justified, with particular emphasis on performing transplants where two DR antigens are shared between donor and recipient.

B-Lymphocytes↗
PubMed1978

Significance of HLA-D/DR matching in renal transplantation.

A low mixed-lymphocyte-culture response, indicating matching for HLA-D, was associated with a relatively good chance of graft survival in 62 recipients of renal transplants from living relatives mismatched for one or two HLA A and/or B antigens. In 96 cadaveric transplants prospectively typed for HLA-DR antigens, compatibility for these antigens improved the prognosis, irrespective of matching for HLA A and B antigens. In cadaveric transplants, a positive B-cell cross-match test before transplantation tended to predict inferior graft survival.

ABO Blood-Group System↗
PubMed1978

Matching for HLA antigens of A, B, and DR loci in renal transplantation by Eurotransplant.

79 patients and their respective cadaveric kidney donors were typed for HLA-A, HLA-B, and HLA-DR antigens using frozen stored spleen lymphocytes and fresh peripheral-blood lymphocytes. The kidney-graft survival-rate at 3 to 18 months was highest when donor and recipient shared one or two DR antigens and three or four A and B antigens. The graft-survival rate was significantly higher (87 +/- 6%) at 18 months in these patients than in less well matched patients (48 +/- 9%).

Epitopes↗
PubMed1978

Lymphocyte subpopulations in man. Expression of HLA-DR determinants on human T cells in infectious mononucleosis.

In a study of lymphocyte subpopulations in peripheral blood during infectious mononucleosis the lymphocytosis was found to be of T-cell origin (i.e. E-RFC), while the number of non T lymphocytes (i.e. EA-, EAC-RFC and SmIg + ve cells) was normal in 7 out of 8 patients. Ten patients were tested for the presence of HLA-DR determinants on their B and T cells and not only B lymphocytes but also a great part (31--75%) of T cells were lysed by the anti HLA-DR testsera, indicating that HLA-DR determinants are expressed on a population of T cells in IM patients. After recovery all patients were retested and showed a normal pattern of HLA-DR typing. This indicates an increase of HLA-DR antigens on T cells or a vigorous proliferation of a small DR-positive T-cell subpopulation during the acute stage of IM.

Absorption↗
PubMed2026

Stage-specific ROMO1 in rheumatoid arthritis: predictive immune insights into the MIF pathway and HLA-DR/IL2RA axis via integrated GWAS, transcriptomic, single-cell, and spatial profiling.

Emerging evidence links reactive oxygen species modulator 1 (ROMO1), a key mitochondrial ROS regulator, to rheumatoid arthritis (RA) pathogenesis. However, its exact mechanism remains elusive given the conflicting evidence about its specific function. We used a four-level integrative framework combining multi-omics data and literature‑supported mechanistic inference. At the genetic level, Mendelian randomization (MR) was performed to explore potential causal relationships between ROMO1, IL2RA, HLA-DR, MIF, and RA risk, followed by differential expression analysis and machine learning-based feature selection to identify key mROS genes. The temporal expression dynamics of ROMO1 were assessed in RA progression. At the cellular and tissue levels, we integrated single-cell RNA sequencing and spatial transcriptomics to map cell-type-specific expression and synovial localization of ROMO1-related immune cells and pathways. Finally, our multi-omics findings were contextualized with literature-supported mechanistic inference. (1) MR results were consistent with a potential protective effect of ROMO1 on RA (OR = 0.52) and its potential regulation of risk factors IL2RA (OR = 0.46) and HLA-DR (OR = 0.40). Conversely, IL2RA (OR = 1.42), HLA-DR (OR = 1.88), and MIF (OR = 1.17) were positively associated with RA risk. Additionally, ROMO1 was identified as a top candidate diagnostic predictor with stage-specific dynamics: downregulated in the early but upregulated in the late/remission stages. (2) Single-cell RNA sequencing showed ROMO1's cell-specific expression in CD14+ HLA-DR+ CD74+ monocytes and CD4+ IL2RA+ T cells. Cell communication analysis further suggested that these cells may participate in MIF pathway regulation. Spatial transcriptomics subsequently identified that ROMO1-related cells localized to synovial pathological regions, with MIF pathway changes correlated with RA progression. (3) Finally, literature-supported mechanistic inference suggests that ROMO1 may modulate mROS levels to promote anti-inflammatory M2 macrophage polarization, which could theoretically contribute to reduced systemic inflammation and the alleviation of multi-organ decline in RA. This integrated multi-omics investigation, supported by literature-based mechanistic inference, suggests ROMO1 as a stage-dependent biomarker candidate and potential immune regulator in RA.

Humans↗
PubMed2004

Ex vivo phenotype and frequency of influenza virus-specific CD4 memory T cells.

Recent advances in class II tetramer staining technology have allowed reliable direct ex vivo visualization of antigen-specific CD4 T cells. In order to define the frequency and phenotype of a prototype response to a nonpersistent pathogen, we have used such techniques to analyze influenza virus-specific memory CD4 T cells directly from blood. These responses are stably detectable ex vivo at low frequencies (range, 0.00012 to 0.0061% of CD4 T cells) and display a distinct "central memory" CD62L(+) phenotype.

CD4-Positive T-Lymphocytes↗
PubMed2026

Genome-wide H3K4me3 profiling of circulating immune cells reveals dynamic epigenetic reprogramming during acute critical COVID-19.

INTRODUCTION: Severe COVID-19 is associated with innate immune dysregulation resembling sepsis-induced immunoparalysis. Epigenetic mechanisms, particularly changes in H3K4me3 enrichment at gene promoters, have been observed in immune tolerance and monocyte dysfunction in sepsis. Whether comparable H3K4me3 alterations occur during acute critical COVID-19 illness has not been investigated. METHODS: In this prospective single-center study, 46 hospitalized COVID-19 patients were enrolled, of whom 27 were treated in the intensive care unit (ICU group) and 19 on the normal ward (non-ICU group). Genome-wide H3K4me3 ChIP-seq was performed on PBMCs at hospital admission (T1) in the total cohort and after seven days (T2) in the ICU group. Monocyte HLA-DR expression and ex vivo TLR-stimulated cytokine secretion were assessed as functional immune readouts. RESULTS: Among 706 differentially bound consensus peaks with promoter association between ICU and non-ICU groups, 704 showed increased H3K4me3 occupancy in ICU patients, predominantly at neutrophil effector gene loci, supported by pathway enrichment of neutrophil degranulation and innate immune activation. Monocyte HLA-DR expression and ex vivo TLR-stimulated IL-6 secretion were persistently reduced throughout the first week of ICU treatment. Longitudinal profiling in the ICU group revealed a shift from an interferon-driven chromatin signature at admission toward sustained innate immune activation and ECM remodeling at day seven. CONCLUSION: This study provides the first genome-wide H3K4me3 characterization of circulating immune cells during acute critical COVID-19, demonstrating that epigenetic reprogramming is an active and dynamic process that mirrors the functional immune dysregulation observed in these patients.

Humans↗
PubMed1978

Possible detection of HLA-DR alloantigenic specificities in man with unabsorbed rabbit antisera.

Thirty-six rabbits were immunized with precipitin lines formed between detergent solubilized membrane fractions from HLA-D-homozygous cells and a rabbit antiserum to human B cells (anti-p 23/30). Thirty-one of the rabbits produced B-cell specific cytotoxic antibodies and twelve of the antibodies were also precipitating in gel diffusion. In cytotoxicity tests six of the antisera showed clear preferential reactivity with the immunizing HLA-D (DR) antigen. Thus immunization of rabbits might prove valuable for the production of HLA-DR typing reagents.

Animals↗
PubMed2026

Glycaemic burden disrupts innate immunity in TB by modulating CD206 expression and macrophage antimicrobial responses.

Tuberculosis (TB) and diabetes mellitus (DM) represent a growing dual global health burden, with chronic hyperglycaemia recognized as a major modifier of host immunity against Mycobacterium tuberculosis (Mtb). Macrophages, central to pathogen recognition, phagocytosis, antigen presentation, and intracellular killing, may be particularly vulnerable to diabetic metabolic dysregulation. This study evaluated phenotypic and functional macrophage alterations in individuals with pulmonary TB, type 2 DM, TB-DM comorbidity, and healthy controls. Surface receptor expression was analysed by multicolour flow cytometry, while phagocytosis and intracellular bacterial clearance were assessed using FITC-labelled Mtb assays and colony-forming unit enumeration. Hyperglycaemia was associated with reduced CD11b, MARCO, and TLR2 expression alongside upregulation of the mannose receptor CD206, which correlated positively with HbA1c levels, indicating a shift toward a permissive M2-like phenotype. Phagocytic uptake of Mtb was significantly impaired and inversely correlated with HbA1c. Antigen-presenting capacity was selectively compromised, with reduced CD80 and CD86 expression in DM and TB-DM groups, while HLA-DR remained unchanged. Intracellular Mtb killing was markedly diminished in diabetic macrophages. These findings demonstrate that chronic hyperglycaemia profoundly disrupts macrophage innate immunity, contributing to increased TB susceptibility and poor infection control in diabetic populations.

Humans↗
PubMed2026

RNF43 Mutations Are Associated With the Classical Molecular Subtype, Vigorous Antitumor Immune Responses, and Prolonged Survival in Pancreatic Adenocarcinoma.

RNF43 mutations were correlated with microsatellite status in colorectal cancer and with fewer and later recurrences in pancreatic ductal adenocarcinoma (PDAC). Here, we undertake a detailed assessment of RNF43 mutations in PDAC. A total of 313 PDACs (308 microsatellite stable [MSS] and 5 microsatellite-instable [MSI] cases) underwent next-generation sequencing (Oncomine Tumor Mutation Load assay; Thermo Fisher). Spatial analyses (NanoString) classified PDACs according to their transcriptomic and proteomic immune signaling. Fluorescent imaging was used to define spatial compartments (tumor: pancytokeratin+/CD45- and leukocytes: pancytokeratin-/CD45+). Each of 20 PDACs with RNF43 mutations (RNF43mut) and without RNF43 mutations (RNF43wt) underwent multiplex immunofluorescence analysis to determine immune status. A total of 153 PDACs (22 RNF43mut and 131 RNF43wt cases) underwent bulk RNA sequencing to assign into molecular subtypes. Overall, 24 RNF43 mutations were identified (22 MSS PDACs and 2 MSI PDACs). The incidence of RNF43 mutations in MSS PDACs (7.1%) was consistent with The Cancer Genome Atlas (6.7%). However, RNF43 mutations were more frequent among MSI PDACs (40%). Additionally, RNF43mut had differential frequencies of other mutations (including Wnt pathway genes), higher tumor mutational burden values (5.5 mut/mb vs 1.67 mut/mb; P < .01), and significantly longer overall survival (47 vs 18 months; P < .0001) than RNF43wt. Moreover, RNF43mut exhibited significantly higher densities of CD8+ T lymphocytes, dendritic cells, and B lymphocytes (P < .001) and an upregulation of ITGAX, CD11c, CD8, and HLA-DR compared with RNF43wt. Patients with RNF43mut PDACs were more often of the classical molecular subtype (20/22, 90.9%). RNF43mut PDACs showed high tumor mutational burden values, suggesting increased neoantigen load coupled with an abundance of antigen-presenting immune cells and an upregulation of immune determinants promoting antigen presentation. All this contributes to stronger antitumor immune responses and improved clinical outcomes.

Humans↗
PubMed2026

Eltrombopag-associated remodeling of the MAIT, MR1+ and &#x3b3;&#x3b4; T cells in pediatric immune thrombocytopenia.

Pediatric immune thrombocytopenia (ITP) is an autoimmune cytopenia characterized by immune-mediated platelet destruction and impaired thrombopoiesis. Mucosa-associated invariant T (MAIT) cells are innate-like T cells activated by MR1-presented microbial metabolites and inflammatory cytokines, but their role in pediatric ITP and their relationship to eltrombopag therapy remain unclear. We analyzed peripheral blood mononuclear cells from healthy controls (n&#xa0;=&#xa0;20), untreated pediatric ITP patients (n&#xa0;=&#xa0;60), and eltrombopag-treated patients (n&#xa0;=&#xa0;16). MAIT cells were quantified using MR1-5-OP-RU tetramers and surrogate gating (CD3+V&#x3b1;7.2+CD161+). MAIT subsets, memory phenotype, chemokine receptor expression (CXCR3, CXCR5, CCR6), HLA-DR, intracellular cytokines (IFN-&#x3b3;, TNF-&#x3b1;, IL-17&#xa0;A, IL-22), and MR1+CD3- cells were analyzed by flow cytometry. Tetramer-defined MAIT cells were reduced in absolute number in pediatric ITP, including eltrombopag-treated patients, most prominently within the CD8+ subset, whereas their frequency among CD3+ T cells did not differ between untreated and eltrombopag-treated groups. In contrast, CD3+V&#x3b1;7.2+CD161+ cells increased in untreated ITP and were lower in eltrombopag-treated patients. Untreated ITP patients exhibited reduced frequencies of IFN-&#x3b3;- and TNF-&#x3b1;-producing MAIT cells, accompanied by increased IL-17-producing cells and TNF-&#x3b1; signal intensity. Conventional &#x3b1;&#x3b2; T cells were reduced, whereas &#x3b3;&#x3b4; T cells were increased; eltrombopag-treated patients exhibited &#x3b3;&#x3b4; T-cell frequencies and cytokine-positive fractions closer to those of healthy controls. MR1+CD3- cells were expanded and displayed reduced HLA-DR expression in untreated ITP, whereas eltrombopag-treated patients showed lower MR1+CD3- frequencies and HLA-DR levels closer to healthy controls. These findings demonstrate coordinated alterations of the MAIT/MR1 axis and unconventional T-cell compartments in pediatric ITP and identify immunophenotypic differences associated with eltrombopag treatment.

Humans↗
PubMed2025

Population analysis and immunologic landscape of melanoma in people living with HIV.

PURPOSE: To dissect the clinical and immunological features of people living with HIV (PLWH) diagnosed with melanoma, who have consistently exhibited worse clinical outcomes than HIV-negative individuals (PLw/oH) with the same cancer. EXPERIMENTAL DESIGN: We analyzed electronic health records from 1,019 PLWH and 373,121 PLw/oH diagnosed with melanoma. Demographic and clinical characteristics were compared. Spatial immune transcriptomics (72 immune-related genes) was performed on melanoma tumor samples (n=11), followed by downstream validation using multiplex immunofluorescence (n=15 PLWH, n=14 PLw/oH). RESULTS: PLWH were diagnosed with melanoma at a younger age, had a higher representation of Hispanic and Black individuals compared to PLw/oH, and a decreased survival rate. PLWH also showed a markedly increased risk of brain metastases. PLWH experienced significant delays in initiating immune checkpoint inhibitor (ICI) therapy and had worse survival outcomes following ICI, even after balancing for demographic covariates. Spatial transcriptomics revealed a more immunosuppressive tumor microenvironment in PLWH, with upregulation of immune checkpoints (PD1, LAG3) and reduced expression of antigen presentation markers (HLA-DRB, B2M), with distinct spatial distributions in tumors and their microenvironments. Multiplex immunofluorescence confirmed an exhausted CD8+ T cell compartment in PLWH, including enrichment of PD1intLAG3- and PD1intLAG3+ subpopulations, and a significant accumulation of immunosuppressive myeloid-derived suppressor cells (CD11b+ HLA-DR- CD33+). CONCLUSIONS: Our findings suggest chronic HIV infection fosters a permissive tumor microenvironment that might undermine effective immune responses and contribute to poor clinical outcomes for PLWH with melanoma. Targeting the actionable immune pathways identified in this study could inform tailored therapeutic strategies to mitigate these disparities.

HIV↗
PubMed1978

A haplotype study of HLA complex with special reference to the HLA-DR series and to Bf. C2 and glyoxalase I polymorphisms.

Fifty-three French families were typed for alleles at seven loci of the HLA complex (HLA-A, -B, -C, -DR, -Bf, -C2 and -GLO) and 212 haplotypes were demonstrated. Eleven recombinations were observed (two A/B, two A/C, two B/Bf, one Bf/D and four D/GLO). The linkage disequilibrium was calculated not only between two alleles (delta) but between three, four...seven alleles (D). In order to compare the intensity of D values in the various haplotypes, the influence of the differences in gene frequencies was eliminated by the introduction of the standardized Ds (Ds = D/D max). The number of haplotypes in disequilibrium is relatively limited since most of the significant Ds involved about 17 haplotypes. For some haplotypes, the disequilibrium covered the whole distance from A to GLO but the stronger disequilibrium concerns the C to Bf or C to DR segment. Three hypotheses (isolation, admixture of population and selection) concerning the formation and maintenance of the disequilibria are discussed.

Epitopes↗