A5042923781- Psoriasis: Treatment and Pathogenesis
- Cytokine Signaling Pathways and Interactions
- Bone Metabolism and Diseases
- Rheumatoid Arthritis Research and Therapies
- Orthopaedic implants and arthroplasty
- Dermatology and Skin Diseases
- Glycosylation and Glycoproteins Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Immune Cell Function and Interaction
- Systemic Lupus Erythematosus Research
- Tissue Engineering and Regenerative Medicine
- RNA regulation and disease
- Hair Growth and Disorders
- Galectins and Cancer Biology
- Dermatological and Skeletal Disorders
- Neutropenia and Cancer Infections
- Surgical Sutures and Adhesives
- Dental Implant Techniques and Outcomes
- Effects of Radiation Exposure
- Autoimmune and Inflammatory Disorders Research
- Monoclonal and Polyclonal Antibodies Research
- IL-33, ST2, and ILC Pathways
- T-cell and B-cell Immunology
- Biomarkers in Disease Mechanisms
- Bone Tissue Engineering Materials
Universitätsklinikum Erlangen
2017-2020
Friedrich-Alexander-Universität Erlangen-Nürnberg
2016-2020
GTx (United States)
1998
BG University Hospital Bergmannsheil Bochum
1998
Monomeric serum immunoglobulin A (IgA) can contribute to the development of various autoimmune diseases, but regulation IgA effector functions is not well defined. Here, we show that two subclasses (IgA1 and IgA2) differ in their effect on immune cells due distinct binding signaling properties. Whereas IgA2 acts pro-inflammatory neutrophils macrophages, IgA1 does have pronounced effects. Moreover, different glycosylation profiles, with possessing more sialic acid than IgA2. Removal increases...
JAK inhibition enhances the function of bone-forming osteoblasts, increases bone mass, and induces repair arthritic erosions.
Generalized pustular psoriasis (GPP) is a severe multi-systemic inflammatory disease characterized by neutrophilic pustulosis and triggered pro-inflammatory IL-36 cytokines in skin. While 19%-41% of affected individuals harbor bi-allelic mutations IL36RN, the genetic cause not known most cases. To identify characterize new pathways involved pathogenesis GPP, we performed whole-exome sequencing 31 with GPP demonstrated effects MPO encoding enzyme myeloperoxidase (MPO). We discovered eight...
Abstract The IL‐1 family member IL‐36α has proinflammatory and pathogenic properties in psoriasis. binds to the IL‐36 receptor leading nuclear factor kappa B/mitogen activated protein kinase mediated cytokine release. IL‐36R antagonist prevents recruitment of accessory therefore IL‐36‐dependent cell activation. In inflamed human tissue, we previously could show that resident B cells plasma (PC) express IL‐36α. Further, fibroblast‐like synoviocytes (FLS) produced cytokines upon...
The phagocyte NADPH oxidase (the NOX2 complex) generates superoxide, the precursor to reactive oxygen species (ROS). ROS possess both antimicrobial and immunoregulatory function. Inactivating mutations in alleles of complex cause chronic granulomatous disease (CGD), characterized by an enhanced susceptibility infections autoimmune diseases such as Systemic lupus erythematosus (SLE). latter is insufficient removal dead cells, resulting response against components cell's nucleus when...
ABSTRACT Enthesitis is a key feature of several different rheumatic diseases. Its pathophysiology only partially known due to the lack access human tissue and shortage reliable animal models for enthesitis. Here, we aimed develop model that mimics effector phase enthesitis reliably leads inflammation new bone formation. was induced by local injection monosodium urate (MSU) crystals into metatarsal entheses wild-type (WT) or oxidative-burst-deficient (Ncf1**) mice. Quantitative variables...
The interleukin (IL)-1 family member IL-33 has been described as intracellular alarmin with broad roles in wound healing, skin inflammation but also autoimmunity. Its dichotomy between full length (fl) and the mature (m) form of its release by necrosis is still not fully understood. Here, we compare functional consequences both forms vivo, therefore generated two lines transgenic mice which selectively overexpress mmIL-33 flmIL-33 basal keratinocytes. Transgene mRNA was expressed at high...
<h3>Career situation of first and presenting author</h3> Student for a master or PhD. <h3>Introduction</h3> Many cytokines relevant to rheumatoid arthritis (RA) rely on the janus kinase – signal transducer activator transcription (JAK-STAT) signaling pathway. The JAK-inhibitors tofacitinib baricitinib, targeting JAK3/JAK1 JAK1/JAK2 respectively, have been approved treatment RA<sup>1</sup>. While currently available therapies reduce inflammation, erosive damage in involved joints is still...
<h3>Background</h3> Targeting cytokines relevant to rheumatoid arthritis (RA) has proven efficient in clinical practice, but there is still demand for therapies that rebuild joint tissues which have been subjected deterioration. Since many involved RA rely on the intracellular janus kinase - signal transducer and activator of transcription (JAK-STAT) signaling pathway, targeting them presents itself as option. For this approach, JAK-inhibitors such Tofacitinib Baricitinib, JAK1/JAK3...