A5040896738- Neuroinflammation and Neurodegeneration Mechanisms
- Complement system in diseases
- Cardiac Imaging and Diagnostics
- Advanced X-ray and CT Imaging
- Atherosclerosis and Cardiovascular Diseases
- Immune Cell Function and Interaction
- T-cell and B-cell Immunology
- Immune cells in cancer
- Circadian rhythm and melatonin
- Radiation Dose and Imaging
- Inflammation biomarkers and pathways
- Medical Imaging Techniques and Applications
- Sleep and related disorders
- Cell Adhesion Molecules Research
- Sleep and Wakefulness Research
- Renal Diseases and Glomerulopathies
- Obstructive Sleep Apnea Research
- Multiple Sclerosis Research Studies
- Galectins and Cancer Biology
- Liver Disease Diagnosis and Treatment
- Systemic Lupus Erythematosus Research
- Apelin-related biomedical research
- Caveolin-1 and cellular processes
- Single-cell and spatial transcriptomics
- Dietary Effects on Health
Medical University of Vienna
2016-2025
Icahn School of Medicine at Mount Sinai
2022-2025
Allen Institute for Brain Science
2023-2025
Siemens (Hungary)
2022-2024
Siemens Healthcare (Germany)
2023-2024
Harvard University
2019-2023
CeMM Research Center for Molecular Medicine
2016-2023
Austrian Academy of Sciences
2016-2023
Center for Systems Biology
2019-2023
Massachusetts General Hospital
2018-2023
Abstract Atherosclerosis is a chronic disease of the vascular wall driven by lipid accumulation and inflammation in intimal layer arteries, its main complications—myocardial infarction stroke—are leading cause mortality worldwide 1,2 . Recent studies have identified triggering receptor expressed on myeloid cells 2 (TREM2), lipid-sensing regulating cell functions 3 , to be highly macrophage foam experimental human atherosclerosis 4 However, role TREM2 not fully known. Here we show that...
While serum-circulating complement destroys invading pathogens, intracellularly active complement, termed the “complosome,” functions as a vital orchestrator of cell-metabolic events underlying T cell effector responses. Whether intracellular is also nonredundant for activity myeloid immune cells currently unknown. Here, we show that monocytes and macrophages constitutively express component (C) 5 generate autocrine C5a via formation an C5 convertase. Cholesterol crystal sensing by induced...
A sleepless night may feel awful in its aftermath, but sleep's revitalizing powers are substantial, perpetuating the idea that convalescent sleep is a consequence-free physiological reset. Although recent studies have shown catch-up insufficiently neutralizes negative effects of debt, mechanisms control prolonged disruption not understood. Here, we show interruption restructures epigenome hematopoietic stem and progenitor cells (HSPCs) increases their proliferation, thus reducing clonal...
HEM1 deficiency causes heritable autoimmunity and immunodeficiency.
Abstract Mice lacking secreted IgM ( sIgM −/− ) antibodies display abnormal splenic B cell development, which results in increased marginal zone and decreased follicular numbers. However, the mechanism by exhibit this effect is unknown. Here, we demonstrate that cells mice receptor (BCR) signaling as judged levels of phosphorylated Bruton’s tyrosine kinase (pBtk), Spleen (pSyk), nuclear Nur77. Low dosage treatment with pBtk inhibitor Ibrutinib reversed altered development spleen mice,...
Monocytes and neutrophils from the myeloid lineage contribute to multiple sclerosis (MS), but dynamics of myelopoiesis during MS are unclear. Here we uncover a disease stage-specific relationship between lifestyle, neuroinflammation. In mice with relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE), in femur, vertebrae spleen is elevated prior onset remission, preceding peaks clinical disability progressive EAE (P-EAE), vertebral rises steadily throughout disease, while...
The immune system is strongly involved in atherosclerosis and regulation generally leads to attenuated atherosclerosis. B- T-lymphocyte attenuator (BTLA) a novel co-receptor that negatively regulates the activation of B T cells; however, there have been no reports BTLA its function or cardiovascular disease (CVD). We aimed assess dominant expressing leucocyte CVD patients investigate whether has functional role experimental atherosclerosis.We show primarily expressed on cells follicular B2...
Abstract Atherosclerosis is a chronic disease of the vascular wall driven by lipid accumulation and inflammation in intimal layer arteries [1], [2], its main complications, myocardial infarction stroke, are leading cause mortality worldwide [3]. Recent studies have identified Triggering receptor expressed on myeloid cells 2 (TREM2), lipid-sensing regulating several key cell functions [4], as highly marker macrophage foam experimental human atherosclerosis [5]. However, function TREM2...
Complement factor H (CFH) has a pivotal role in regulating alternative complement activation through its ability to inhibit the cleavage of central component C3, which links innate and humoral immunity. However, insights into CFH B cell biology are limited. Here, we demonstrate that deficiency mice leads altered splenic development characterized by accumulation marginal zone (MZ) cells. Furthermore, cells Cfh-/- exhibit enhanced receptor (BCR) signaling as evaluated increased levels...
Obtaining accurate coronary artery calcium (CAC) score measurements from CCTA datasets with virtual non-iodine (VNI) algorithms would reduce acquisition time and radiation dose. We aimed to assess the agreement of VNI-derived conventional true non-contrast (TNC)-based CAC scores identify predictors accuracy.CCTA were acquired either 120 or 140 kVp. volumes calculated TNC VNI images in 197 consecutive patients undergoing CCTA. density score, mean volume/lesion, aortic Hounsfield units...
B and T cells are interconnected in the follicular helper—germinal center cell (T FH -GC cell) axis, which is hyperactive during atherosclerosis development loss of control along this axis results exacerbated atherosclerosis. Inhibition –GC can be achieved by providing negative co-stimulation to through PD-1/PD-L1 pathway. Therefore, we investigated a novel therapeutic strategy using PD-L1-expressing inhibit We found that IFNγ-stimulated significantly enhanced PD-L1 expression limited...