{"id":7008,"date":"2023-05-08T14:24:30","date_gmt":"2023-05-08T12:24:30","guid":{"rendered":"https:\/\/www.izkf.med.fau.de\/?page_id=7008"},"modified":"2025-09-04T13:55:01","modified_gmt":"2025-09-04T11:55:01","slug":"gefoerderte-projekte","status":"publish","type":"page","link":"https:\/\/www.izkf.med.fau.de\/en\/elan\/anschubfinanzierung\/gefoerderte-projekte\/","title":{"rendered":"Current Pilot Projects"},"content":{"rendered":"<div class=\"cris\"><div class=\"cris-fields\"><h2>ELAN-Pilot Projects<\/h2><p>ELAN pilot projects provide funds for junior researchers (postdocs, until the age of 39 (i.e. before the 39th birthday) at the time of application).<br \/><\/p><h3>Projects: <\/h3><div class=\"rrze-elements accordion style_default\" id=\"accordion-0\">\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_0\" aria-expanded=\"false\" aria-controls=\"collapse_0\" id=\"collapse_button_0\"> P164: Define the role of Annexins as ligands of Dectin-1 regulating osteoclast differentiation <\/button><\/h2>\n<div id=\"collapse_0\" class=\"accordion-body\" aria-labelledby=\"collapse_button_0\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. May 2025 - 30. October 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Bettina Gr\u00f6tsch<\/span><\/p>\n<p class=\"abstract\">Our preliminary results suggest that AnnexinA1, which is expressed by dying cells within the bone marrow niche, will bind to Dectin-1 on osteoclasts to induce osteoclast differentiation and bone resorption in non-inflammatory conditions. Therefore, I will analyse the molecular mechanism of AnnexinA1 induced Dectin-1 signaling. Furthermore, I aim to define the AnnexinA1 expressing myeloid cell population within the bone marrow niche and its impact on osteoclast differentiation.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/353992263?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_1\" aria-expanded=\"false\" aria-controls=\"collapse_1\" id=\"collapse_button_1\"> P168: Crosstalk between T cells subtypes and fibroblast subsets in skin autoimmunity <\/button><\/h2>\n<div id=\"collapse_1\" class=\"accordion-body\" aria-labelledby=\"collapse_button_1\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>21. February 2025 - 20. August 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Aleix Rius Rigau<\/span><\/p>\n<p class=\"abstract\">Skin autoimmunity consist in an aberrant immune response involving complex interactions between immune and stromal cells. Systemic sclerosis (SSc) is a skin autoimmune disorder with primary fibrotic components. Distinct fibroblasts subsets relevant in SSc have been identified, but to date is not known their spatial relationships with immune cells. Their role in SLE is also unknown. We plan to use a spatial multi-omics approach to better understand these processes.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/354169568?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_2\" aria-expanded=\"false\" aria-controls=\"collapse_2\" id=\"collapse_button_2\"> P174: Endometrial Cancer \u0096 New molecular classification in a Real-world data Evaluation <\/button><\/h2>\n<div id=\"collapse_2\" class=\"accordion-body\" aria-labelledby=\"collapse_button_2\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. August 2025 - 31. July 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Patrik P\u00f6schke<\/span><\/p>\n<p class=\"abstract\">The application aims to investigate endometrial cancers with regard to new molecular classifications. The ENCORE project studies real-world survival based on molecular patterns, analyzes the immune environment of tumors with concurrent p53 mutations, and correlates the eosinophil to lymphocyte ratio with patient outcome. In addition, the relevance of hormone and HER2 receptors in the individual molecular subtypes is examined.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/336803114?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_3\" aria-expanded=\"false\" aria-controls=\"collapse_3\" id=\"collapse_button_3\"> P176: Garcinol as a new therapeutic option for chondrosarcoma <\/button><\/h2>\n<div id=\"collapse_3\" class=\"accordion-body\" aria-labelledby=\"collapse_button_3\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. June 2025 - 30. November 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Sebastian St\u00e4bler<\/span><\/p>\n<p class=\"abstract\">Chondrosarcomas are malignant bone tumors, which do not respond to existing chemo- and radiotherapy. Preliminary studies could show that the the natural compound Garcinol strongly reduces proliferation and colony formation of these tumor cells. Additionally, Garcinol could re-sensitize chondrosarcoma cells to the chemotherapeutic Cisplatin. We therefore want to investigate the role of Garcinol as a new therapeutic option for chondrosarcoma.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/336803981?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_4\" aria-expanded=\"false\" aria-controls=\"collapse_4\" id=\"collapse_button_4\"> P179: Muscle tissue engineering on PCL collagen I-PANi nanofiber scaffolds in the EPI loop model <\/button><\/h2>\n<div id=\"collapse_4\" class=\"accordion-body\" aria-labelledby=\"collapse_button_4\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. August 2025 - 31. January 2027<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Lilly Mengen<\/span><\/p>\n<p class=\"abstract\">The aim of this project is to generate differentiated, axially vascularized and neurotized skeletal muscle tissue from ADSC and myoblasts on PCL-collagen I-(PANi)-nanofiber scaffolds. For this, seeded nanofiber scaffolds of PCL-collagen I with and without Polyanilin (4%) will be implanted in the neurotized vascular loop model of the rat for 6 weeks. Afterwards the myogenic differentiation will be analysed with the hypothesis, that the addition of PANi (4%) improves myogenic differentiation.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/354109808?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_5\" aria-expanded=\"false\" aria-controls=\"collapse_5\" id=\"collapse_button_5\"> P180: Investigation of the role of AP-1 transcription factors in melanoma dormancy in a 3D-printed model <\/button><\/h2>\n<div id=\"collapse_5\" class=\"accordion-body\" aria-labelledby=\"collapse_button_5\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>15. September 2025 - 14. September 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Sonja Schmidt<\/span><\/p>\n<p class=\"abstract\">In this project, the role of the AP-1 transcription factors in tumor dormancy of malignant melanoma is investigated. Using our 3D biofabricated dormancy model, we could show that AP-1 factors are highly expressed in dormant melanoma cells. Additionally, preliminary data indicate an impact of AP-1 factors on the development of dormancy. To shed more light on the phenomenon of tumor dormancy, the role of AP-1 and respective signaling pathways will be analyzed in our 3D printed model system.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/353781735?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_6\" aria-expanded=\"false\" aria-controls=\"collapse_6\" id=\"collapse_button_6\"> P181: Reciprocal control of metabolism and immunomodulation in adipose tissue and liver <\/button><\/h2>\n<div id=\"collapse_6\" class=\"accordion-body\" aria-labelledby=\"collapse_button_6\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. July 2025 - 31. December 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Andreas Wild<\/span><\/p>\n<p class=\"abstract\">Obesity is marked by excessive lipid accumulation, leading to chronic inflammation in adipose tissue (AT), due to an increase in inflammatory immune cells causing insulin resistance and fat accumulation in other organs like the liver. This project focuses on the role of the immunomodulatory CD83 molecule in in lipid metabolism and obesity-related immune regulation in AT and the liver, potentially providing insights for new therapeutic strategies against obesity.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/347996163?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_7\" aria-expanded=\"false\" aria-controls=\"collapse_7\" id=\"collapse_button_7\"> P184: Establishing a Kidney Organoid Model for Complement Research in Acute Kidney Injury <\/button><\/h2>\n<div id=\"collapse_7\" class=\"accordion-body\" aria-labelledby=\"collapse_button_7\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. August 2025 - 31. July 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Eva Vonbrunn<\/span><\/p>\n<p class=\"abstract\">The aim of this project is to establish a kidney organoid model to study complement activation in acute kidney injury. The model will first be optimized in terms of complexity and structure. Once established the kidney organoids will be used for co-culture experiments with immune cells, a hypoxia model of acute kidney injury and studies of the complement system. The development of the renal organoid model will contribute to the understanding of signalling pathways and therapeutic strategies.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/347995911?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_8\" aria-expanded=\"false\" aria-controls=\"collapse_8\" id=\"collapse_button_8\"> P190: Investigation of EVs\u0092 protective role in developing intestine of zebrafish larvae <\/button><\/h2>\n<div id=\"collapse_8\" class=\"accordion-body\" aria-labelledby=\"collapse_button_8\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. December 2025 - 30. November 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Linda-Marie Mulzer<\/span><\/p>\n<p class=\"abstract\">Extracellular vesicles (EVs) are membrane-bound nanoparticles essential for cell communication and organogenesis. We hypothesize that human breast milk-derived EVs (HBM-EVs) enhance intestinal maturation and regeneration. This study investigates HBM-EV protection in DSS-induced intestinal injury in zebrafish larvae, analyzing cell-morphology, inflammation, and tissue repair (Phalloidin, cleaved Caspase-3, TNF-?, Wnt5a), comparing EVs from three lactation stages.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/353782249?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_9\" aria-expanded=\"false\" aria-controls=\"collapse_9\" id=\"collapse_button_9\"> P177: Generation of Synthetic Contrast-Enhanced Breast-MR Images From Native Sequences Using Deep Learning <\/button><\/h2>\n<div id=\"collapse_9\" class=\"accordion-body\" aria-labelledby=\"collapse_button_9\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. November 2025 - 30. October 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Lorenz Kapsner<\/span><\/p>\n<p class=\"abstract\">The application of Latent Diffusion Models (LDMs) in the context of breast MRI is being investigated, aiming to generate synthetic contrast-enhanced (CE) subtraction sequences of the breast by using native MRI sequences as input for the conditioning process. The resulting images will be evaluated regarding their suitability for diagnostic  purposes. The results will help to better understand the potential and limits of LDMs in the context of generating synthetical CE breast MRI.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/358877650?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_10\" aria-expanded=\"false\" aria-controls=\"collapse_10\" id=\"collapse_button_10\"> P178: Integrative analysis of single-cell RNA-seq data to unravel CAF subtypes in PDAC mouse models <\/button><\/h2>\n<div id=\"collapse_10\" class=\"accordion-body\" aria-labelledby=\"collapse_button_10\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. February 2026 - 31. January 2027<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Renato Liguori<\/span><\/p>\n<p class=\"abstract\">This project aims to develop a robust reference framework for CAF subtypes analysis by integrating scRNA-seq datasets from PDAC mouse models. By identifying consistent gene signatures, we will provide a foundation for studying CAF heterogeneity and their function in PDAC. The resulting dataset will enhance reproducibility in preclinical research and facilitate future studies of CAF dynamics in diverse tumor contexts.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/353784181?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_11\" aria-expanded=\"false\" aria-controls=\"collapse_11\" id=\"collapse_button_11\"> P189: Generation of recombinant vaccine candidates against BoDV-1 <\/button><\/h2>\n<div id=\"collapse_11\" class=\"accordion-body\" aria-labelledby=\"collapse_button_11\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. January 2026 - 31. December 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Dominik Damm<\/span><\/p>\n<p class=\"abstract\">Borna Disease Virus 1 (BoDV-1) causes fatal encephalitis in humans. This project aims to generate recombinant variants of the glycoprotein G via structure-guided vaccine design. The G variants will be conjugated to the surface of liposomes that incorporate biomolecular adjuvants to boost immunogenicity. Optionally, we aim to mimic a live-attenuated vaccine by additional encapsulation of viral structural proteins. The BoDV-1 liposomes would be used in future studies with antibody-humanized mice.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/355529390?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_12\" aria-expanded=\"false\" aria-controls=\"collapse_12\" id=\"collapse_button_12\"> P186: PAINMAP-IBD: Skin Sensory Testing to Assess Visceral Nerve Dysfunction in IBD-related Abdominal Pain <\/button><\/h2>\n<div id=\"collapse_12\" class=\"accordion-body\" aria-labelledby=\"collapse_button_12\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. January 2026 - 31. December 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Miriam D\u00fcll<\/span><\/p>\n<div class=\"person-card\">\n<div class=\"fau-person card-xsmall shrink-contact person-card\">\n<div class=\"card-item card-xsmall shrink-contact\" itemscope itemtype=\"http:\/\/schema.org\/Person\">\n<figure itemprop=\"image\" class=\"person-thumb\" aria-hidden=\"true\" role=\"presentation\" itemtype=\"http:\/\/schema.org\/ImageObject\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-250x300.jpg\" itemprop=\"contentUrl\" alt=\"Miriam D\u00fcll\" srcset=\"https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-250x300.jpg 250w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-853x1024.jpg 853w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-768x922.jpg 768w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-1279x1536.jpg 1279w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-50x60.jpg 50w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-92x110.jpg 92w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-200x240.jpg 200w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-267x320.jpg 267w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell-391x470.jpg 391w, https:\/\/www.izkf.med.fau.de\/files\/2022\/12\/duell.jpg 1635w\"><meta itemprop=\"width\" content=\"250\"><meta itemprop=\"height\" content=\"300\"><\/figure>\n<h3><a href=\"https:\/\/www.izkf.med.fau.de\/person\/miriam-duell\/\"><span itemprop=\"name\"><span itemprop=\"honorificPrefix\">Dr.<\/span> <span class=\"fullname\"><span itemprop=\"givenName\">Margareta Miriam<\/span> <span itemprop=\"familyName\">D\u00fcll<\/span><\/span><\/span><\/a><\/h3>\n<\/div>\n<\/div>\n<\/div>\n<p class=\"abstract\">PAINMAP-IBD explores whether cutaneous sensory afferents can serve as a surrogate marker of visceral nerve dysfunction in IBD-associated abdominal pain. Using abdominal quantitative sensory testing (QST) and C-fiber-selective stimulation, the project characterizes sensory phenotypes and peripheral neurofunction. Findings will be correlated with clinical activity, biomarkers, and treatment response across defined patient cohorts.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/353832433?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_13\" aria-expanded=\"false\" aria-controls=\"collapse_13\" id=\"collapse_button_13\"> P188_OA: Allospecific Responses of Marginal Zone B Cells in Kidney Transplantation <\/button><\/h2>\n<div id=\"collapse_13\" class=\"accordion-body\" aria-labelledby=\"collapse_button_13\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. March 2026 - 28. February 2027<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Louisa Steines<\/span><\/p>\n<p class=\"abstract\">Rejection is a major cause of allograft failure. The role of marginal zone B cells in kidney transplantation is unkown. In this project, we will investigate the donor-specific responses of marginal zone B cells using a rat kidney transplantat model. Specifically, we will determine the capacity of marginal zone B cells to produce anti-donor antibodies, to secrete inflammatory or regulatory cytokines and the sensitivity towards anti-BAFF antibody treatment in a kidney transplant model.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/358877948?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_14\" aria-expanded=\"false\" aria-controls=\"collapse_14\" id=\"collapse_button_14\"> P195: On the role and consequence of LINE-1 retroelements in extracellular vesicles <\/button><\/h2>\n<div id=\"collapse_14\" class=\"accordion-body\" aria-labelledby=\"collapse_button_14\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. January 2026 - 31. December 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Thomas Gramberg<\/span><\/p>\n<div class=\"person-card\">\n<div class=\"fau-person card-xsmall shrink-contact person-card\">\n<div class=\"card-item card-xsmall shrink-contact\" itemscope itemtype=\"http:\/\/schema.org\/Person\">\n<figure itemprop=\"image\" class=\"person-thumb\" aria-hidden=\"true\" role=\"presentation\" itemtype=\"http:\/\/schema.org\/ImageObject\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-250x300.jpg\" itemprop=\"contentUrl\" alt=\"Prof. Dr. Thomas Gramberg\" srcset=\"https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-250x300.jpg 250w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-853x1024.jpg 853w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-768x922.jpg 768w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-1280x1536.jpg 1280w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-50x60.jpg 50w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-92x110.jpg 92w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-200x240.jpg 200w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-267x320.jpg 267w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg-392x470.jpg 392w, https:\/\/www.izkf.med.fau.de\/files\/2023\/02\/gramberg.jpg 1649w\"><meta itemprop=\"width\" content=\"250\"><meta itemprop=\"height\" content=\"300\"><\/figure>\n<h3><a href=\"https:\/\/www.izkf.med.fau.de\/person\/prof-dr-thomas-gramberg\/\"><span itemprop=\"name\"><span itemprop=\"honorificPrefix\">Prof. Dr.<\/span> <span class=\"fullname\"><span itemprop=\"givenName\">Thomas<\/span> <span itemprop=\"familyName\">Gramberg<\/span><\/span><\/span><\/a><\/h3>\n<\/div>\n<\/div>\n<\/div>\n<p class=\"abstract\">LINE-1 retroelements (L1) are upregulated in many autoimmune diseases, including  SLE. Although L1 replicates intracellularly, we found L1 RNA packaged in extracellular vesicles (EV) in sera from SLE patients. Since L1 nucleic acids can trigger inflammatory pathways, we hypothesize that L1-EVs impact pathogenesis and could be used as novel biomarker in patients. Also, we ask whether L1 can be mobilized via EVs, challenging the dogma of L1s as intracellular pathogen.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/360898472?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_15\" aria-expanded=\"false\" aria-controls=\"collapse_15\" id=\"collapse_button_15\"> P183: Molecular characterisation of the remission mediated by CAR T cells in Systemic Lupus Erythematosus <\/button><\/h2>\n<div id=\"collapse_15\" class=\"accordion-body\" aria-labelledby=\"collapse_button_15\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. January 2026 - 31. December 2026<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Panagiotis Garantziotis<\/span><\/p>\n<p class=\"abstract\">Despite progress in understanding SLE, remission is rare. A \"treat-to-target\" approach aims to minimize disease activity, reducing organ damage and flares. B-cell immunity transcriptional signature correlates with treatment response, with effective therapy requiring its reversal. CAR T cells show promise for sustained, drug-free remission. Here, we will delineate transcriptional fingerprints of treatment response and resistance to uncover molecular drivers of effective therapy and remission.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/361203381?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_16\" aria-expanded=\"false\" aria-controls=\"collapse_16\" id=\"collapse_button_16\"> P194: GPR15-mediated trafficking of antibody-secreting cells in IBD <\/button><\/h2>\n<div id=\"collapse_16\" class=\"accordion-body\" aria-labelledby=\"collapse_button_16\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. June 2026 - 31. May 2027<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Sebastian Schramm<\/span><\/p>\n<p class=\"abstract\">This project investigates the effects of GPR15:GPR15L on the gut-homing of antibody-secreting cells in context of inflammatory bowel disease. It studies the differential influence of this trafficking programme on IgA\/IgG-producing cells and whether a modulation of this mechanism affects intestinal inflammatory processes and the composition of the gut microbiome. Therefore, in vitro and in vivo assays will be performed combined with transcriptomic and metagenomic data analyses.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/363178268?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_17\" aria-expanded=\"false\" aria-controls=\"collapse_17\" id=\"collapse_button_17\"> P197: Investigating the Sequence Grammar of Age-Sensitive cis-Regulatory Elements in Neuronal Aging <\/button><\/h2>\n<div id=\"collapse_17\" class=\"accordion-body\" aria-labelledby=\"collapse_button_17\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. July 2026 - 30. June 2027<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Angel Josue Cerecedo Castillo<\/span><\/p>\n<p class=\"abstract\">Why do some gene-control switches in neurons fail with age while others remain stable? Using genome-wide measurements of RNA, chromatin accessibility, and histone marks, we will map age-sensitive regulatory DNA in neurons and learn the sequence rules that predict vulnerability. Interpretable AI models will nominate key motifs and combinations, which we will test by targeted sequence edits and reporter assays in neuronal systems to pinpoint causal mechanisms and candidate intervention points.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/363964299?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"accordion-group\">\n<h2 class=\"accordion-heading\"><button class=\"accordion-toggle\" data-toggle=\"collapse\"  href=\"#collapse_18\" aria-expanded=\"false\" aria-controls=\"collapse_18\" id=\"collapse_button_18\"> P196: Role of the transcription factor cJun in eosinophil effector function during allergic inflammation <\/button><\/h2>\n<div id=\"collapse_18\" class=\"accordion-body\" aria-labelledby=\"collapse_button_18\">\n<div class=\"accordion-inner clearfix\"><strong>Term: <\/strong>1. June 2026 - 31. May 2027<br \/><strong>Project leader: <\/strong><span class=\"author\" itemprop=\"author\">Tatiana Albarracin Melo<\/span><\/p>\n<p class=\"abstract\">Eosinophils are key drivers of allergic airway inflammation. The transcription factor AP-1 (c-Jun) regulates many immune cells, yet its specific role in eosinophils remains unknown. Using eosinophil-specific c-Jun knockout mice, we will analyze how c-Jun controls eosinophil activation, migration, and survival in allergy models, aiming to identify novel therapeutic targets.<\/p>\n<p>&#8594; <a href=\"https:\/\/cris.fau.de\/projects\/364623598?lang=en_GB\">More information<\/a> <\/p>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div><\/div>\n\n\n\n<p class=\"wp-block-paragraph\"><\/p>\n","protected":false},"excerpt":{"rendered":"","protected":false},"author":1355,"featured_media":1920,"parent":6971,"menu_order":4,"comment_status":"closed","ping_status":"closed","template":"page-templates\/page-subnav.php","meta":{"_rrze_cache":"enabled","_access_permission":"","_rrze_multilang_single_locale":"en_GB","_rrze_multilang_single_source":"https:\/\/www.izkf.med.fau.de\/?page_id=1793","_faue_teaser_image_id":0,"footnotes":""},"page_category":[],"page_tag":[],"workflow_usergroup":[],"class_list":["post-7008","page","type-page","status-publish","has-post-thumbnail","hentry","en-GB"],"faue_teaser_image_url":"","_links":{"self":[{"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/pages\/7008","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/users\/1355"}],"replies":[{"embeddable":true,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/comments?post=7008"}],"version-history":[{"count":6,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/pages\/7008\/revisions"}],"predecessor-version":[{"id":109357,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/pages\/7008\/revisions\/109357"}],"up":[{"embeddable":true,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/pages\/6971"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/media\/1920"}],"wp:attachment":[{"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/media?parent=7008"}],"wp:term":[{"taxonomy":"page_category","embeddable":true,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/page_category?post=7008"},{"taxonomy":"page_tag","embeddable":true,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/page_tag?post=7008"},{"taxonomy":"workflow_usergroup","embeddable":true,"href":"https:\/\/www.izkf.med.fau.de\/wp-json\/wp\/v2\/workflow_usergroup?post=7008"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}