{"title":"[Donor lymphocyte infusion after allogeneic stem cell transplantation].","authors":"Christoph Schmid, Hans-Jochem Kolb","doi":"10.1007/s00108-025-01948-8","DOIUrl":"https://doi.org/10.1007/s00108-025-01948-8","url":null,"abstract":"<p><p>The transfusion of donor lymphocytes after allogeneic stem cell transplantation (known as donor lymphocyte infusion, DLI) is the oldest form of cellular immunotherapy. The therapeutic effect is based on the polyclonal reaction of the transferred immune effector cells of the donor against the underlying malignant disease, the graft versus malignancy reaction (GvM). Based on findings from the canine model, DLI has been used for over 30 years, primarily for the prophylaxis and treatment of recurrence of hematological neoplasms after allogeneic transplantation, whereby the various diseases exhibit very different sensitivities to the GvM effect. As a result, both the indications and the potential combination of DLI with classical chemotherapy and newer drugs are different. The main complication of DLI is the induction of a graft versus host disease, the risk of which is influenced in particular by the human leukocyte antigen (HLA) match between donor and recipient as well as the dosage and timing of DLI. Based on large registry data, recommendations for the implementation of DLI in the various constellations and indications have been developed in recent years, which have already proven to be easy to implement in practice. This article summarizes the basic principles, clinical use and recommendations for application.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144546459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Fibrotic diseases in the gastrointestinal tract : Liver fibrosis and more].","authors":"Elke Roeb","doi":"10.1007/s00108-025-01869-6","DOIUrl":"10.1007/s00108-025-01869-6","url":null,"abstract":"<p><p>Chronic liver damage, such as metabolic dysfunction-associated steatotic liver disease (MASLD), viral hepatitis B or C, cholestatic hepatitis (PBC, PSC), toxic damage (alcohol) or genetic alterations (hemochromatosis, Wilson's disease, etc.) usually cause a chronic inflammatory response in liver cells or bile duct epithelial cells. In the long term this chronic inflammatory response can lead to scarring of the liver, a condition known as fibrosis. The development of liver fibrosis is largely independent of the causative agent, although the pattern of initial fibrosis (periportal, pericentral or sinusoidal) can vary. Untreated and progressive fibrosis can sometimes lead to complete architectural deconstruction and deposition of connective tissue in the liver, intestines and other parenchymal organs, with a gradual loss of function. In the end stage of liver cirrhosis, portal hypertension, encephalopathy, bleeding or carcinomas, e.g., hepatocellular carcinoma (HCC) and intrahepatic cholangiocellular carcinoma (iCCCa), can occur. Intestinal fibrosis is one of the most devastating complications of Crohn's disease. With novel and consistent therapeutic interventions, fibrotic processes can be stopped and reversed. New research technologies have substantially improved our knowledge of liver fibrogenesis and intestinal fibrosis. The focus of this review article is on MASLD and Crohn's disease, chronic inflammatory diseases of the liver and intestines with increasing prevalence and a major impact on the general population. The current principles and potential possibilities of preventive and therapeutic antifibrotic interventions are illustrated.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"695-701"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143544756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Pathophysiology of fibrosis: inflammatory vs. non-inflammatory].","authors":"Elena Neumann, Philipp Klemm","doi":"10.1007/s00108-025-01890-9","DOIUrl":"10.1007/s00108-025-01890-9","url":null,"abstract":"<p><p>Fibrosis is characterized by an excessive accumulation of extracellular matrix components produced by connective tissue cells. It is a pathophysiological feature of many chronic inflammatory diseases. Nearly every tissue of the body can be affected by fibrosis. Its progression can lead to dysfunction of the affected tissue and organs and potentially death. Early fibrotic mechanisms include the activation of immune responses leading to activation of connective tissue cells and misdirected wound healing responses, finally leading to scarring and fibrosis. Different pathways and factors contribute to the pathophysiology of fibrosis and are summarized in this review.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"659-665"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Blood vessels as a target organ: from Ormond's disease to immunoglobulin G4-related diseases].","authors":"Marco Krasselt, Bimba Hoyer","doi":"10.1007/s00108-025-01891-8","DOIUrl":"10.1007/s00108-025-01891-8","url":null,"abstract":"<p><p>Immunoglobulin G4-related disease (IgG4-RD) is a rare and clinically diverse entity with an estimated incidence of 0.8-1.4 per 100,000 person-years. Typical sites of manifestation include the head and neck area, the hepato-pancreato-biliary system, and the retroperitoneum. Perhaps the best-known variant is retroperitoneal fibrosis, formerly known as Ormond's disease. Biopsy and histological examination are of great diagnostic importance, as relying solely on serum IgG4 is problematic and not sufficiently specific. Therapeutically, in addition to the initial administration of glucocorticoids, treatment with B cell-directed antibodies, particularly rituximab, has become clinically established. Initial studies demonstrate the effectiveness of other therapies targeting B cells. Although the disease has received more clinical attention in recent years, it is still necessary to further increase awareness of IgG4-RD to enable optimal treatment for patients.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"686-694"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Pharmacological inhibition of fibrosis exemplified by systemic sclerosis : Possibilities and limits].","authors":"Tobias Dashi, Christina Bergmann","doi":"10.1007/s00108-025-01925-1","DOIUrl":"10.1007/s00108-025-01925-1","url":null,"abstract":"<p><p>Fibrotic diseases, such as cardiac, liver and lung fibrosis are a heterogeneous group of diseases with high mortality and fatality rates. Identifying cross-disease mechanisms is a potential strategy to find targets for these sometimes rare diseases. Additionally, it is necessary to consider disease-specific differences. Systemic sclerosis (SSc) is an autoimmune, fibrotic systemic disease. The possibilities and limitations of the pharmacological inhibition of fibrosis are exemplified and discussed in this article using SSc as an example. The focus of the article is on relevant pathogenetic aspects, new insights into known therapeutic principles, emerging developments \"on the way to clinical application and ongoing studies\", as well as an outlook on open questions. Continuing innovations in the field of molecular biological and computer-assisted analytical methods are enabling an increasingly more precise understanding of fibrosing tissue processes, serving as a basis for identifying new treatment strategies and approaches. Numerous targeted therapies are currently in phase 2/phase 3 clinical trials and are expected to be concluded in the coming years. Additionally, innovative options for deep B‑cell depletion are available for clinical testing; however, a \"cure\" for fibrotic diseases has not yet been achieved, and further questions remain on the research agenda.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"702-711"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144509819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"[Target organ the lungs: diversity of fibrotic pulmonary diseases].","authors":"Gabriela Leuschner, Jürgen Behr","doi":"10.1007/s00108-025-01911-7","DOIUrl":"10.1007/s00108-025-01911-7","url":null,"abstract":"<p><strong>Background: </strong>Fibrotic lung diseases are part of the large and heterogeneous group of interstitial lung diseases (ILD), which are characterized by a progressive fibrotic remodelling of alveolar lung parenchyma.</p><p><strong>Objective: </strong>Overview of the spectrum of fibrotic lung diseases.</p><p><strong>Material and methods: </strong>A literature search was carried out in the PubMed and MEDLINE database.</p><p><strong>Results: </strong>The etiology of fibrotic ILD is diverse and includes inhaled exogenous noxious substances (dust, gases), infections, drug reactions, ionizing radiation and endogenous autoimmune or rare genetically determined metabolic and storage disorders; however, the etiology of some ILDs, so-called idiopathic interstitial pneumonia (IIP), is not fully understood although environmental pollution, tobacco smoke and genetic polymorphisms have been identified as risk factors. The most important and best studied representative of IIP is idiopathic pulmonary fibrosis (IPF). The diagnosis of ILD is complex and requires an interdisciplinary approach taking the clinical presentation, radiological patterns, and possibly bronchoalveolar lavage and histological findings into account. Characteristic of progressive fibrotic lung disease is progressive fibrotic tissue remodeling, which is manifested as clinical, functional and radiological deterioration and is referred to as progressive pulmonary fibrosis (PPF). Antifibrotic drugs delay the progression of IPF and PPF but are not curative.</p><p><strong>Discussion: </strong>In addition to early diagnosis and preventive strategies, a better understanding of the causes of fibrotic ILD is required in order to avoid triggering noxious agents, identify dysregulated signalling pathways and develop targeted treatment.</p>","PeriodicalId":73385,"journal":{"name":"Innere Medizin (Heidelberg, Germany)","volume":" ","pages":"666-677"},"PeriodicalIF":0.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144487377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}