Daniela Čiháková

ORCID: 0000-0002-8713-2860
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About
Contact & Profiles
Research Areas
  • Viral Infections and Immunology Research
  • Immune Cell Function and Interaction
  • Cardiac Fibrosis and Remodeling
  • Eosinophilic Disorders and Syndromes
  • T-cell and B-cell Immunology
  • Atherosclerosis and Cardiovascular Diseases
  • IL-33, ST2, and ILC Pathways
  • CAR-T cell therapy research
  • Cytokine Signaling Pathways and Interactions
  • Cancer Immunotherapy and Biomarkers
  • Eosinophilic Esophagitis
  • Cytomegalovirus and herpesvirus research
  • Celiac Disease Research and Management
  • COVID-19 Clinical Research Studies
  • Microscopic Colitis
  • Long-Term Effects of COVID-19
  • Whipple's Disease and Interleukins
  • Immune cells in cancer
  • Diabetes and associated disorders
  • Cardiovascular Effects of Exercise
  • Systemic Lupus Erythematosus Research
  • Galectins and Cancer Biology
  • Tryptophan and brain disorders
  • Cardiomyopathy and Myosin Studies
  • Adrenal Hormones and Disorders

Johns Hopkins University
2015-2024

Johns Hopkins Medicine
2015-2024

Lund University
2023

University of Baltimore
2007-2021

Johns Hopkins Bayview Medical Center
2021

Bloomberg (United States)
2015-2020

Massachusetts General Hospital
2019-2020

University of Maryland, Baltimore
2019-2020

University of South Carolina
2020

Carleton College
2020

Rationale : One-third of myocarditis cases progresses to dilated cardiomyopathy (DCM), but the mechanisms controlling this process are largely unknown. CD4 + T helper (Th)17 cells have been implicated in pathogenesis autoimmune diseases, role Th17-produced cytokines during inflammation-induced cardiac remodeling has not previously studied. Objective We examined importance interleukin (IL)-17A progression DCM using a mouse model. Methods and Results Immunization mice with myocarditogenic...

10.1161/circresaha.109.213157 article EN Circulation Research 2010-04-09

Abstract Recent clinical studies have reinforced the importance of sex-related differences in pathogenesis cardiovascular diseases, with an increased incidence and mortality men. Similar to humans, male BALB/c mice infected coxsackievirus B3 (CVB3) develop more severe inflammation heart even though viral replication is no greater than females. We show that TLR4 IFN-γ levels are significantly elevated regulatory T cell (Treg) populations reduced males following CVB3 infection, whereas females...

10.4049/jimmunol.178.11.6710 article EN The Journal of Immunology 2007-06-01

Inflammatory dilated cardiomyopathy (DCMi) is a major cause of heart failure in individuals below the age 40. We recently reported that IL-17A required for development DCMi. show novel pathway connecting IL-17A, cardiac fibroblasts (CFs), GM-CSF, and heart-infiltrating myeloid cells with pathogenesis Il17ra−/− mice were protected from DCMi, this was associated significantly diminished neutrophil Ly6Chi monocyte/macrophage (MO/MΦ) infiltrates. Depletion MO/MΦ also Mechanistically, stimulated...

10.1084/jem.20132126 article EN cc-by-nc-sa The Journal of Experimental Medicine 2014-06-16

Medical devices and implants made of synthetic materials can induce an immune-mediated process when implanted in the body called foreign response, which results formation a fibrous capsule around implant. To explore immune stromal connections underpinning we analyzed fibrotic capsules surrounding surgically excised human breast from 12 individuals. We found increased numbers interleukin 17 (IL17)-producing γδ+ T cells CD4+ helper (TH17) as well senescent capsules. Further analysis murine...

10.1126/scitranslmed.aax3799 article EN Science Translational Medicine 2020-04-15

Inflammatory dilated cardiomyopathy (DCMi) is a major cause of heart failure in children and young adults. DCMi develops up to 30% myocarditis patients, but the mechanisms involved disease progression are poorly understood. Patients with eosinophilia frequently develop cardiomyopathies. In this study, we used experimental autoimmune (EAM) model determine role eosinophils DCMi. Eosinophils were dispensable for induction required Eosinophil-deficient ΔdblGATA1 mice, contrast WT showed no signs...

10.1084/jem.20161702 article EN cc-by-nc-sa The Journal of Experimental Medicine 2017-03-16

Immune checkpoint inhibitors (ICIs) are an effective therapy for various cancers; however, they can induce immune-related adverse events (irAEs) as a side effect. Myocarditis is uncommon, but fatal, irAE caused after ICI treatments. Currently, the mechanism of ICI-associated myocarditis unclear. Here, we show development in A/J mice induced by anti-PD-1 monoclonal antibody (mAb) administration alone without tumor cell inoculation, immunization, or viral infection. Mice with have increased...

10.1016/j.celrep.2022.111611 article EN cc-by-nc-nd Cell Reports 2022-11-01

Myocarditis and myopericarditis may occur after COVID-19 vaccination with an incidence of two to twenty cases per 100,000 individuals, but underlying mechanisms related disease onset progression remain unclear. Here, we report a case following the first dose mRNA-1273 vaccine in young man who had history mild three months before vaccination. The patient presented chest pain, elevated troponin I level, electrocardiogram abnormality. His endomyocardial biopsy revealed diffuse CD68+ cell...

10.3389/fimmu.2022.851620 article EN cc-by Frontiers in Immunology 2022-02-18

Immune checkpoint inhibitors (ICIs) are specialized monoclonal antibodies (mAbs) that target immune checkpoints and their ligands, counteracting cancer cell-induced T-cell suppression. Approved ICIs like cytotoxic T-lymphocyte antigen-4 (CTLA-4), programmed death-1 (PD-1), its ligand PD-L1, lymphocyte activation gene-3 (LAG-3) have improved patient outcomes by enhancing anti-tumor responses. However, some patients unresponsive, others experience immune-related adverse events (irAEs),...

10.3389/fimmu.2024.1340373 article EN cc-by Frontiers in Immunology 2024-02-05

Autoimmunity significantly contributes to the pathogenesis of myocarditis, underscored by its increased frequency in autoimmune diseases such as systemic lupus erythematosus and polymyositis. Even cases myocarditis caused viral infections, dysregulated immune responses contribute pathogenesis. However, whether triggered existing conditions or precise antigens immunologic pathways driving remain incompletely understood. The emergence associated with checkpoint inhibitor therapy, commonly used...

10.1161/circresaha.124.323816 article EN Circulation Research 2024-06-06

Abstract Autoimmune diseases can be reduced or even prevented if proinflammatory immune responses are appropriately down-regulated. Receptors (such as CTLA-4), cytokines TGF-β), and specialized cells CD4+CD25+ T regulatory cells) work together to keep in check. cell Ig mucin (Tim) family proteins key regulators of inflammation, providing an inhibitory signal that dampens thereby reducing autoimmune allergic responses. We show this study Tim-3 signaling during the innate response viral...

10.4049/jimmunol.176.11.6411 article EN The Journal of Immunology 2006-06-01

The involvement of macrophages (MΦs) in Th17-cell responses is still poorly understood. While neutrophils are thought to be the predominant effector responses, IL-17 also known induce myelotropic chemokines and growth factors. Other T-cell-derived cytokines non-classical functions, suggesting that sigxnaling may similarly elicit unique MΦ functions. Here, we characterized expression subunits receptor on primary murine MΦs from different anatomical compartments. greatest receptors was...

10.1002/eji.201141737 article EN European Journal of Immunology 2011-12-12

Myocarditis is a leading cause of sudden cardiac failure in young adults. Natural killer (NK) cells, subset the innate lymphoid cell compartment, are protective viral myocarditis. Herein, we demonstrated that these qualities extend to suppressing autoimmune inflammation. Experimental myocarditis (EAM) was initiated BALB/c mice by immunization with myocarditogenic peptide. During EAM, activated NK cells secreted interferon γ, perforin, and granzyme B, expressed CD69, tumor necrosis...

10.1016/j.ajpath.2014.11.023 article EN cc-by-nc-nd American Journal Of Pathology 2015-01-24

Myocarditis is a major cause of heart failure and sudden cardiac death in young adults adolescents. Many cases myocarditis are associated with autoimmune processes which myosin autoantigen. Conventional immunosuppressive therapies often provide unsatisfactory results adverse toxicities during the treatment myocarditis. Cannabidiol (CBD) nonpsychoactive constituent marijuana that exerts antiinflammatory effects independent classical cannabinoid receptors. Recently, 80 clinical trials have...

10.2119/molmed.2016.00007 article EN cc-by Molecular Medicine 2016-01-01

Cardiac manifestations are a major cause of morbidity and mortality in patients with eosinophil-associated diseases. Eosinophils thought to play pathogenic role myocarditis. We investigated the pathways that recruit eosinophils heart using model eosinophilic myocarditis, which experimental autoimmune myocarditis (EAM) is induced IFNγ-/- IL-17A-/- mice. Two conditions necessary for efficient eosinophil trafficking heart: high eotaxin (CCL11, CCL24) expression receptor CCR3 by eosinophils....

10.1002/eji.201646557 article EN European Journal of Immunology 2016-09-13

Two types of monocytes, Ly6Chi and Ly6Clo, infiltrate the heart in murine experimental autoimmune myocarditis (EAM). We discovered a role for cardiac fibroblasts facilitating monocyte-to-macrophage differentiation both Ly6Clo cells, allowing these macrophages to perform divergent functions progression. During acute phase EAM, IL-17A is highly abundant. It signals through attenuate efferocytosis monocyte-derived (MDMs) simultaneously prevents differentiation. demonstrated an inverse clinical...

10.1016/j.celrep.2019.06.007 article EN cc-by-nc-nd Cell Reports 2019-07-01
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