Éva Korpos

ORCID: 0000-0002-0438-4211
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About
Contact & Profiles
Research Areas
  • Diabetes and associated disorders
  • Pancreatic function and diabetes
  • Cell Adhesion Molecules Research
  • Diabetes Management and Research
  • Protease and Inhibitor Mechanisms
  • Proteoglycans and glycosaminoglycans research
  • Muscle Physiology and Disorders
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Barrier Structure and Function Studies
  • Tissue Engineering and Regenerative Medicine
  • T-cell and B-cell Immunology
  • Immunotherapy and Immune Responses
  • Ion channel regulation and function
  • Liver physiology and pathology
  • Blood Coagulation and Thrombosis Mechanisms
  • Immune Response and Inflammation
  • Immune Cell Function and Interaction
  • Bone Metabolism and Diseases
  • Immune cells in cancer
  • Osteoarthritis Treatment and Mechanisms
  • Cardiac electrophysiology and arrhythmias
  • S100 Proteins and Annexins
  • Hepatitis C virus research
  • Orthopaedic implants and arthroplasty
  • Peptidase Inhibition and Analysis

University of Münster
2009-2025

University of Debrecen
2022-2025

HUN-REN Szegedi Biológiai Kutatóközpont
2005-2014

Hungarian Academy of Sciences
2000-2014

Institute of Biochemistry
2000-2014

University of Szeged
2007

Although chemokines are sufficient for chemotaxis of various cells, increasing evidence exists their fine-tuning by selective proteolytic processing. Using a model immune cell into the CNS (experimental autoimmune encephalomyelitis [EAE]) that permits precise localization immigrating leukocytes at blood-brain barrier, we show that, whereas required leukocyte migration CNS, additional MMP-2/9 activities specifically border parenchyma strongly enhance this transmigration process. Cytokines...

10.1016/j.celrep.2015.01.037 article EN cc-by-nc-nd Cell Reports 2015-02-01

We provide the first comprehensive analysis of extracellular matrix (ECM) composition peri-islet capsules, composed basement membrane (BM) and subjacent interstitial (IM), in development type 1 diabetes NOD mice human diabetes. Our data demonstrate global loss BM IM components only at sites leukocyte infiltration into islet. Stereological analyses reveal a correlation between incidence insulitis number islets showing versus with intact BMs, suggesting that penetration is critical step....

10.2337/db12-0432 article EN cc-by-nc-nd Diabetes 2012-11-09

The enzymes gelatinase A/matrix metalloproteinase-2 (MMP-2) and B/MMP-9 are essential for induction of neuroinflammatory symptoms in experimental autoimmune encephalomyelitis (EAE), a mouse model multiple sclerosis (MS); the absence these enzymes, disease does not develop. We therefore investigated cellular sources relative contributions MMP-2 MMP-9 to at early stages EAE induction. demonstrated that from an immune cell source is required initial infiltration leukocytes into central nervous...

10.1126/scitranslmed.aaf8020 article EN Science Translational Medicine 2016-11-09

Inactivating mutations of the NF-κB essential modulator (NEMO), a key component signaling, cause genetic disease incontinentia pigmenti (IP). This leads to severe neurological symptoms, but mechanisms underlying brain involvement were unclear. Here, we show that selectively deleting Nemo or upstream kinase Tak1 in endothelial cells resulted death cells, rarefaction microvessels, cerebral hypoperfusion, disrupted blood–brain barrier (BBB), and epileptic seizures. TAK1 NEMO protected BBB by...

10.1084/jem.20150165 article EN The Journal of Experimental Medicine 2015-09-07

Abstract An important regulatory suppressive function in autoimmune and other inflammatory processes has been ascribed to CD4+Foxp3+ T cells (Tregs), which requires direct cell-cell communication between Tregs, effector cells, APCs. However, the molecular basis for these interactions not yet clarified. We show here that sialoadhesin (Sn), prototype of siglec family sialic acid-binding transmembrane proteins, expressed by resident activated tissue-infiltrating macrophages, directly binds...

10.4049/jimmunol.0804247 article EN The Journal of Immunology 2009-05-04

Abstract Aims/hypothesis We and others previously reported the presence of tertiary lymphoid organs (TLOs) in pancreas NOD mice, where they play a role development type 1 diabetes. Our aims here are to investigate whether TLOs present individuals with diabetes characterise their distinctive features, comparison mouse pancreases, order interpret functional significance. Methods Using immunofluorescence confocal microscopy, we examined extracellular matrix (ECM) cellular constituents...

10.1007/s00125-021-05453-z article EN cc-by Diabetologia 2021-04-29

Type 1 diabetes (T1D) is a chronic autoimmune disease that results from T cell-mediated destruction of pancreatic β cells. CD1d-restricted NKT lymphocytes have the ability to regulate immunity, including autoimmunity. We previously demonstrated type II cells, which carry diverse TCRs, prevented T1D in NOD mouse model for human disease. In this study, we show CD4(+) 24αβ but not CD4/CD8 double-negative were sufficient downregulate diabetogenic BDC2.5 cells adoptive transfer experiments....

10.4049/jimmunol.1101390 article EN The Journal of Immunology 2012-02-28

Very late antigen 4 (VLA-4; integrin α4β1) is critical for transmigration of T helper (TH) 1 cells into the central nervous system (CNS) under inflammatory conditions such as multiple sclerosis (MS). We have previously shown that VLA-4 and melanoma cell adhesion molecule (MCAM) are important trans-endothelial migration human TH17 in vitro here investigate their contribution to pathogenic CNS inflammation.Antibody blockade MCAM assessed murine models inflammation conjunction with conditional...

10.1186/s12974-018-1276-4 article EN cc-by Journal of Neuroinflammation 2018-08-22

In autoimmune Type 1 diabetes (T1D), immune cells infiltrate and destroy the islets of Langerhans — islands endocrine tissue dispersed throughout pancreas. However, contribution cellular programs outside to insulitis is unclear. Here, using CO-Detection by indEXing (CODEX) imaging cadaveric pancreas samples, we simultaneously examine islet extra-islet inflammation in human T1D. We identify four sub-states inflamed characterized activation profiles CD8 + T enriched relative surrounding...

10.7554/elife.100535.2 preprint EN 2025-03-06

In autoimmune type 1 diabetes (T1D), immune cells infiltrate and destroy the islets of Langerhans — islands endocrine tissue dispersed throughout pancreas. However, contribution cellular programs outside to insulitis is unclear. Here, using CO-Detection by indEXing (CODEX) imaging cadaveric pancreas samples, we simultaneously examine islet extra-islet inflammation in human T1D. We identify four sub-states inflamed characterized activation profiles CD8 + T enriched relative surrounding...

10.7554/elife.100535.3 article EN cc-by eLife 2025-04-15

Biglycan, a small leucine rich proteoglycan, is expressed in almost every tissue of the body, mainly extracellular matrix connective tissues. Although there an increasing amount data on biological role biglycan protein, its function still poorly understood. We aimed to gather more information about protein cardiac tissues, and signal transduction. Therefore, we generated transgenic mice overexpressing human analyzed profile offsprings using quantitative real-time (QRT)-PCR proteomics....

10.1021/pr060571b article EN Journal of Proteome Research 2007-01-18

Here we identify a role for the matrilin-2 (Matn2) extracellular matrix protein in controlling early steps of myogenic differentiation. We observed Matn2 deposition around proliferating, differentiating and fusing myoblasts culture during muscle regeneration vivo. silencing delayed expression Cdk inhibitor p21 Nfix, MyoD, Myog genes, explaining retarded cell cycle exit myoblast rescue restored differentiation genes. TGF-β1 inhibited at least part by repressing expression, which onset...

10.1242/jcs.141556 article EN cc-by Journal of Cell Science 2014-01-01
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