A5067641587- Immune Cell Function and Interaction
- Immune Response and Inflammation
- T-cell and B-cell Immunology
- Cytokine Signaling Pathways and Interactions
- Immunotherapy and Immune Responses
- Psoriasis: Treatment and Pathogenesis
- IL-33, ST2, and ILC Pathways
- Cancer Immunotherapy and Biomarkers
- Immune cells in cancer
- Neuroinflammation and Neurodegeneration Mechanisms
- Cell death mechanisms and regulation
- ATP Synthase and ATPases Research
- Whipple's Disease and Interleukins
- Mitochondrial Function and Pathology
- Pluripotent Stem Cells Research
- NF-κB Signaling Pathways
- Reproductive System and Pregnancy
- Inflammasome and immune disorders
- Cancer-related molecular mechanisms research
- Medicinal Plant Pharmacodynamics Research
- Fungal Infections and Studies
- Atherosclerosis and Cardiovascular Diseases
- Heme Oxygenase-1 and Carbon Monoxide
- Antifungal resistance and susceptibility
- Inflammation biomarkers and pathways
University Medical Center of the Johannes Gutenberg University Mainz
2014-2024
Johannes Gutenberg University Mainz
2014-2024
University of California, San Francisco
2018-2020
Engelhardt Institute of Molecular Biology
2009-2018
Lomonosov Moscow State University
2011-2014
Russian Academy of Sciences
2008
Institute of Gene Biology
2007
Liver metastasis suppresses systemic tumor-specific immunity and contributes to the resistance checkpoint immunotherapy.
Candidalysin, a hypha-associated fungal peptide, drives interleukin-17 responses to Candida albicans .
Significance In spite of TNF involvement in the pathogenesis multiple sclerosis (MS), systemic neutralization MS patients was not successful. One possible reasons is that possesses both pathogenic and protective features may be related to TNFR1 versus TNFR2 receptor engagement. This study uncovers one such functions mediated by intrinsic signaling T reg cells. mice bearing humanized genetic loci, ablation restricted cells led reduced capacity control Th17 cell responses, exacerbated...
Interleukin-17A- (IL-17A) and IL-17F-producing CD4+ T helper cells (TH17 cells) are implicated in the development of chronic inflammatory diseases, such as multiple sclerosis its animal model, experimental autoimmune encephalomyelitis (EAE). TH17 also orchestrate leukocyte invasion central nervous system (CNS) subsequent tissue damage. However, role IL-17A IL-17F effector cytokines is still confused with encephalitogenic function that produce these cytokines, namely, cells, fueling a...
The proinflammatory cytokine interleukin 1 (IL-1) is crucially involved in the pathogenesis of multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE). Herein, we studied role IL-1 signaling blood-brain barrier (BBB) endothelial cells (ECs), astrocytes microglia for EAE development, using mice with conditional deletion receptor IL-1R1. We found that redundant development EAE, whereas IL-1R1 BBB-ECs markedly ameliorated disease severity. upregulated...
Significance Smad7 is a negative regulator of TGF-β signaling, cytokine with anti-inflammatory properties. Although was implicated in the development and function dendritic cells (DCs), vivo role DCs remains elusive. Here, we demonstrate that DC-specific deletion affects splenic CD8 + CD103 by regulating expression transcription factors Batf3 IRF8. In addition, directs DC indoleamine 2,3-dioxygenase response to IFN-γ signaling. Hence, absent mediates resistance mice autoimmunity via...
The cytokine interleukin-6 (IL-6) plays a central role in the inflammation cascade as well cardiovascular disease progression. Since myeloid cells are primary source of IL-6 formation, we aimed to generate mouse model study cell-derived vascular disease.
Abstract Bcl-3 is an atypical NF-κB family member that regulates NF-κB-dependent gene expression in effector T cells, but a cell-intrinsic function regulatory (Treg) cells and colitis not clear. Here we show levels colonic correlate with disease manifestation patients inflammatory bowel disease. Mice T-cell-specific overexpression of develop severe can be attributed to defective Treg cell development function, leading the infiltration immune such as pro-inflammatory γδT αβ cells. In...
IL-1 is a key cytokine known to drive chronic inflammation and regulate many physiological, immunological, neuroimmunological responses via actions on diverse cell types of the body. To determine mechanisms as part inflammatory response in vivo, we generated conditional receptor 1 (IL-1R1) mouse mutant using Cre/LoxP system (IL-1R1(fl/fl) ). In generated, exon 5, which encodes extracellular-binding region receptor, flanked by LoxP sites, thereby inactivating two previously described...
Interleukin-1 (IL-1) plays a crucial role in numerous inflammatory diseases via action on its only known signaling IL-1 receptor type 1 (IL-1R1). To investigate the of selected cell types, we generated new mouse strain which exon 5 Il1r1 gene is flanked by loxP sites. Crossing these mice with CD4-Cre transgenic resulted IL-1R1 loss function specifically T cells. These mice, termed IL-1R1ΔT, displayed normal development under steady state conditions. Importantly, isolated CD4 positive cells...
The function of NF‐κB family members is controlled by multiple mechanisms including the transcriptional regulator Bcl‐3, an atypical member IκB family. By using a murine model conditional Bcl‐3 overexpression specifically in T cells, we observed impairment development Th2, Th1, and Th17 cells. High expression promoted CD4 + T‐cell survival, but at same time suppressed proliferation response to TCR stimulation, resulting reduced expansion. As consequence, T‐cell‐specific led inflammation...
IL-6 binds to the IL-6R α-chain (IL-6Rα) and signals via signal transducer gp130. Recently, was found also bind cell surface glycoprotein CD5, which would then engage gp130 in absence of IL-6Rα. However, biological relevance this alternative pathway is under debate. In study, we developed a mouse model, murine overexpressed CD11c-Cre-dependent manner. Transgenic mice lethal immune dysregulation syndrome with increased numbers Ly-6G+ neutrophils Ly-6Chi monocytes/macrophages. overexpression...
Prenatal imprinting to interleukin 17A (IL-17A) triggers behavioral disorders in offspring. However, reported models of maternal immune activation utilizing immunostimulants, lack specificity elucidate the anatomical compartments IL-17A's action and distinct disturbances it causes. By combining transgenic IL-17A overexpression with deficiency its receptor, we established a novel model prenatal (acronym: PRIMA-17 model). This allowed us study exclusively through embryo-restricted responses....