Eszter Lázár‐Molnár

ORCID: 0000-0003-0802-9409
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Renal Transplantation Outcomes and Treatments
  • Immunodeficiency and Autoimmune Disorders
  • Immunotherapy and Immune Responses
  • Cancer Immunotherapy and Biomarkers
  • Monoclonal and Polyclonal Antibodies Research
  • Mast cells and histamine
  • Biosimilars and Bioanalytical Methods
  • Cytomegalovirus and herpesvirus research
  • Inflammatory Bowel Disease
  • Fungal Infections and Studies
  • Polyamine Metabolism and Applications
  • Immune Response and Inflammation
  • Tuberculosis Research and Epidemiology
  • Drug-Induced Adverse Reactions
  • Asthma and respiratory diseases
  • Chronic Lymphocytic Leukemia Research
  • Systemic Lupus Erythematosus Research
  • Renal and Vascular Pathologies
  • Mechanical Circulatory Support Devices
  • Microscopic Colitis
  • Renal Diseases and Glomerulopathies
  • Chemokine receptors and signaling
  • Cancer Genomics and Diagnostics

ARUP Laboratories (United States)
2014-2025

University of Utah
2016-2025

ARUP Institute for Clinical and Experimental Pathology
2017-2019

University of Utah Health Care
2017-2018

Albert Einstein College of Medicine
2006-2017

United States University
2017

Bipar
2007-2008

Semmelweis University
2000-2002

Christie's
2002

University of Debrecen
2002

The programmed death-1 (PD-1) costimulatory receptor inhibits T and B cell responses plays a crucial role in peripheral tolerance. PD-1 has recently been shown to inhibit during chronic viral infections such as HIV. In this study, we examined the of infection with Mycobacterium tuberculosis , common co-infection PD-1–deficient mice showed dramatically reduced survival compared wild-type mice. lungs −/− uncontrolled bacterial proliferation focal necrotic areas predominantly neutrophilic...

10.1073/pnas.1007394107 article EN Proceedings of the National Academy of Sciences 2010-07-12

Programmed death-1 (PD-1) is a member of the CD28/B7 superfamily that delivers negative signals upon interaction with its two ligands, PD-L1 or PD-L2. The high-resolution crystal structure complex formed by complete ectodomains murine PD-1 and PD-L2 revealed 1:1 receptor:ligand stoichiometry displayed binding interface overall molecular organization distinct from observed in CTLA-4/B7 inhibitory complexes. Furthermore, our also provides insights into association between highlights...

10.1073/pnas.0804453105 article EN Proceedings of the National Academy of Sciences 2008-07-19

Many hematopoietic cell types express CD1d and are capable of presenting glycolipid antigens to invariant natural killer T cells (iNKT cells). However, the question which principal presenters in vivo remains controversial, it has been suggested that this might vary depending on structure a particular antigen. Here we have shown single type cell, CD8α+ DEC-205+ dendritic was mainly responsible for capturing variety different antigens, including multiple forms α-galactosylceramide stimulate...

10.1016/j.immuni.2013.12.004 article EN cc-by Immunity 2014-01-01

The PD-1 costimulatory receptor inhibits T cell signaling upon interacting with its ligands PD-L1 and PD-L2. PD-1/PD-L pathway is critical in maintaining self-tolerance. In this study, we examined the role of a mouse model acute infection Histoplasma capsulatum, major human pathogenic fungus. lethal histoplasmosis, all PD-1-deficient mice survived infection, whereas wild-type died disseminated disease. PD-L expression on macrophages splenocytes was up-regulated during from infected inhibited...

10.1073/pnas.0711918105 article EN Proceedings of the National Academy of Sciences 2008-02-12

B7-H1 (PD-L1) on immune cells plays an important role in T cell coinhibition by binding its receptor PD-1. Here, we show that both human and mouse intestinal epithelium express B7-H1-deficient mice are highly susceptible to dextran sodium sulfate (DSS)- or trinitrobenzenesulfonic acid (TNBS)-induced gut injury. deficiency during inflammation leads high mortality morbidity, which associated with severe pathological manifestations the colon, including loss of epithelial integrity overgrowth...

10.1016/j.celrep.2014.01.020 article EN cc-by Cell Reports 2014-02-01

Programmed Cell Death-1 (PD-1) is an inhibitory immune receptor, which plays critical roles in T cell co-inhibition and exhaustion upon binding to its ligands PD-L1 PD-L2. We report the crystal structure of human PD-1 ectodomain mapping interface. Mutagenesis studies confirmed crystallographic interface, resulted mutant receptors with altered affinity ligand-specificity. In particular, a high-affinity (HA PD-1) exhibited 45 30-fold increase PD-L2, respectively, due slower dissociation rates....

10.1016/j.ebiom.2017.02.004 article EN cc-by EBioMedicine 2017-02-06

Abstract Background Immunoassays based on label-free technologies (label-free immunoassay [LFIA]) offer an innovative approach to clinical diagnostics and demonstrate great promise for therapeutic drug monitoring (TDM) of monoclonal antibody (mAb) drugs. An LFIA measures immunocomplex formation in real time allows quantification initial binding rate, which facilitates fast measurement within a few minutes. Methods Based thin-film interferometry (TFI) technology, open-access LFIAs were...

10.1093/clinchem/hvaa179 article EN Clinical Chemistry 2020-07-16

Monoclonal antibodies (MAbs) to a cell surface histone on Histoplasma capsulatum modify murine infection and decrease the growth of H. within macrophages. Without MAbs, survives macrophages by modifying intraphagosomal environment. In present study, we aimed analyze affects MAb macrophage phagosomes. Using transmission electron fluorescence microscopy, showed that phagosome activation maturation are significantly greater when yeast opsonized with MAb. The reduced ability organism regulate...

10.1128/ec.00036-08 article EN Eukaryotic Cell 2008-05-17

Abstract Implementation of human leukocyte antigen ( HLA ) genotyping by next‐generation sequencing NGS in the clinical lab brings new challenges to laboratories performing this testing. With advent commercially available HLA‐NGS typing kits, labs must make numerous decisions concerning capital equipment and address labor considerations. Therefore, careful unbiased evaluation methods is imperative. In report, we compared our in‐house developed with two kits from Illumina Omixon using 10...

10.1111/tan.12850 article EN HLA 2016-07-01

Abstract Background Interleukin‐6 (IL‐6) is a bifunctional growth factor in malignant melanoma; its expression increases during the progression of disease. Histamine, detected large amounts normal and pathological proliferating tissues, an important paracrine autocrine regulator tumour cell proliferation as well. Materials methods We investigated presence function IL‐6 histamine WM35 primary human melanoma line with respect to their direct role regulatory interactions. Results inhibited...

10.1046/j.1365-2362.2002.01020.x article EN European Journal of Clinical Investigation 2002-10-01

Background. HLA-DQ mismatch has been identified as a predictor of de novo donor-specific HLA antibody formation and antibody-mediated rejection. There are insufficient data to guide the incorporation DQ into organ allocation decisions. Methods. We used retrospective longitudinal cohort adult living donor kidney transplant recipients from 11 centers across United States for whom high-resolution class II typing was available. HLA-DQαβ heterodimer allele quantified all donor-recipient pairs,...

10.1097/tp.0000000000005198 article EN Transplantation 2024-09-05

Histidine decarboxylase (HDC) is the single enzyme responsible for histamine synthesis. HDC-deficient mice (HDC(-/-)) have no in their tissues when kept on a histamine-free diet. Therefore, HDC(-/-) provide suitable model to investigate involvement of regulation receptor expression. Gene expression H1 and H2 receptors was studied several organs compared standard (HDC(+/+)) mice. In many tissues, prolonged absence induced down-regulation subtype. The less sensitive deficiency. Exogenous...

10.1016/s0014-5793(01)03070-8 article EN FEBS Letters 2001-10-31
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