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Article ; Online: IL-10 revisited in systemic lupus erythematosus.

Biswas, Swayanka / Bieber, Katja / Manz, Rudolf Armin

2022 Volume 13, Page(s) 970906

Abstract: IL-10 is a cytokine with pleiotropic functions, particularly known for its suppressive effects on various immune cells. Consequently, it can limit the pathogenesis of inflammatory diseases, such as multiple sclerosis (MS), inflammatory bowel disease, ... ...

Abstract	IL-10 is a cytokine with pleiotropic functions, particularly known for its suppressive effects on various immune cells. Consequently, it can limit the pathogenesis of inflammatory diseases, such as multiple sclerosis (MS), inflammatory bowel disease, Crohn's disease, and Epidermolysis bullosa acquisita, among others. Recent evidence however indicates that it plays dual roles in Systemic lupus Erythematosus (SLE) where it may inhibit pro-inflammatory effector functions but seems to be also a main driver of the extrafollicular antibody response, outside of germinal centers (GC). In line, IL-10 promotes direct differentiation of activated B cells into plasma cells rather than stimulating a GC response. IL-10 is produced by B cells, myeloid cells, and certain T cell subsets, including extrafollicular T helper cells, which are phenotypically distinct from follicular helper T cells that are relevant for GC formation. In SLE patients and murine lupus models extrafollicular T helper cells have been reported to support ongoing extrafollicular formation of autoreactive plasma cells, despite the presence of GCs. Here, we discuss the role of IL-10 as driver of B cell responses, its impact on B cell proliferation, class switch, and plasma cells.
MeSH term(s)	Animals ; B-Lymphocytes ; Germinal Center ; Humans ; Interleukin-10 ; Lupus Erythematosus, Systemic ; Mice ; T-Lymphocytes, Helper-Inducer
Chemical Substances	Interleukin-10 (130068-27-8)
Language	English
Publishing date	2022-08-01
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.970906
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Article ; Online: Drug Development in Pemphigoid Diseases.

Bieber, Katja / Ludwig, Ralf J

Acta dermato-venereologica

2020 Volume 100, Issue 5, Page(s) adv00055

Abstract: Pemphigoid diseases are organ-specific autoimmune diseases of the skin and/or mucous membranes. They are caused by autoantibodies targeting adhesion molecules located at the dermal-epidermal junction. While the diagnostics of pemphigoid diseases and ... ...

Abstract	Pemphigoid diseases are organ-specific autoimmune diseases of the skin and/or mucous membranes. They are caused by autoantibodies targeting adhesion molecules located at the dermal-epidermal junction. While the diagnostics of pemphigoid diseases and insights into their pathogenesis have improved significantly, the development of novel treatments that are effective and safe remains an unmet medical need. However, numerous pre-clinical studies and early clinical trials have recently been launched. This review summarizes some pathways leading to drug development in pemphigoid diseases, namely: (i) hypothesis-driven drug development; (ii) omics-based drug development; (iii) drug repurposing; (iv) screening-based drug development; and (v) drug development based on careful clinical observations. Ultimately, it is hoped that this will lead to personalized and curative treatments.
MeSH term(s)	Autoantibodies/drug effects ; Autoimmune Diseases/drug therapy ; Autoimmune Diseases/pathology ; Cell Adhesion Molecules/immunology ; Dimethyl Fumarate/therapeutic use ; Doxycycline/therapeutic use ; Drug Development ; Epidermolysis Bullosa Acquisita/drug therapy ; Epidermolysis Bullosa Acquisita/immunology ; Epidermolysis Bullosa Acquisita/pathology ; Female ; Forecasting ; Humans ; Male ; Molecular Targeted Therapy/methods ; Pemphigoid, Bullous/drug therapy ; Pemphigoid, Bullous/immunology ; Pemphigoid, Bullous/pathology ; Protein-Tyrosine Kinases/administration & dosage ; Skin Diseases, Vesiculobullous/drug therapy ; Skin Diseases, Vesiculobullous/immunology ; Skin Diseases, Vesiculobullous/pathology ; Translational Research, Biomedical
Chemical Substances	Autoantibodies ; Cell Adhesion Molecules ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Dimethyl Fumarate (FO2303MNI2) ; Doxycycline (N12000U13O)
Language	English
Publishing date	2020-02-12
Publishing country	Sweden
Document type	Journal Article ; Review
ZDB-ID	80007-7
ISSN	1651-2057 ; 0001-5555
ISSN (online)	1651-2057
ISSN	0001-5555
DOI	10.2340/00015555-3400
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Book ; Online ; Thesis: Die Rolle von regulatorischen T Zellen in der Effektorphase der Epidermolysis bullosa acquisita

Groß, Natalie [Verfasser] / Bieber, Katja [Akademischer Betreuer] / Redecke, Lars [Akademischer Betreuer]

2024

Author's details	Natalie Groß ; Akademische Betreuer: Katja Bieber, Lars Redecke
Keywords	Naturwissenschaften ; Science
Subject code	sg500
Language	German
Publisher	Zentrale Hochschulbibliothek Lübeck
Publishing place	Lübeck
Document type	Book ; Online ; Thesis
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Article ; Online: Risk of comorbid autoimmune diseases in patients with immunobullous disorders: A global large-scale cohort study.

Kasperkiewicz, Michael / Vorobyev, Artem / Bieber, Katja / Kridin, Khalaf / Ludwig, Ralf J

Journal of the American Academy of Dermatology

2023 Volume 89, Issue 6, Page(s) 1269–1271

MeSH term(s)	Humans ; Cohort Studies ; Pemphigus ; Pemphigoid, Bullous ; Skin Diseases ; Autoimmune Diseases/complications ; Autoimmune Diseases/epidemiology
Language	English
Publishing date	2023-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603641-7
ISSN	1097-6787 ; 0190-9622
ISSN (online)	1097-6787
ISSN	0190-9622
DOI	10.1016/j.jaad.2023.07.1030
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Article ; Online: Risk factors and sequelae of epidermolysis bullosa acquisita: A propensity-matched global study in 1,344 patients.

Kridin, Khalaf / Vorobyev, Artem / Papara, Cristian / De Luca, David A / Bieber, Katja / Ludwig, Ralf J

Frontiers in immunology

2023 Volume 13, Page(s) 1103533

Abstract: Identification of risk factors and sequelae of any given disease is of key importance. For common diseases, primary prevention and disease management are based on this knowledge. For orphan diseases, identification of risk factors and sequelae has been ... ...

Abstract	Identification of risk factors and sequelae of any given disease is of key importance. For common diseases, primary prevention and disease management are based on this knowledge. For orphan diseases, identification of risk factors and sequelae has been challenging. With the advent of large databases, e.g., TriNetX, this can now be addressed. We used TriNetX to identify risk factors and sequelae of epidermolysis bullosa acquisita (EBA), a severe and orphan autoimmune disease. To date, there is only enigmatic information on EBA comorbidity. We recruited 1,344 EBA patients in the Global Collaborative Network of TriNetX. Using the "explore outcomes" function we identified 55 diagnoses with a different prevalence between EBA and no-EBA patients. We next performed propensity-matched, retrospective cohort studies in which we determined the risk of EBA development following any of the identified 55 diseases. Here, 31/55 diseases were identified as risk factors for subsequent EBA. Importantly, the highest risk for EBA were other chronic inflammatory diseases (CID), especially lupus erythematosus and lichen planus. Lastly, we determined the risk to develop any of the identified diseases after EBA diagnosis. Here, 38/55 diseases were identified as sequelae. Notably, EBA patients showed an increased risk for metabolic and cardiovascular disease, and thrombosis. Furthermore, the risk for CIDs, especially lupus erythematosus and lichen planus, was elevated. These insights into risk factors and sequelae of EBA are not only of clinical relevance, e.g., optimizing cardiovascular disease risk, but in addition, point to shared pathogenetic pathways between EBA and other inflammatory diseases.
MeSH term(s)	Humans ; Epidermolysis Bullosa Acquisita/complications ; Epidermolysis Bullosa Acquisita/epidemiology ; Retrospective Studies ; Cardiovascular Diseases/complications ; Lupus Erythematosus, Systemic/diagnosis ; Disease Progression ; Lichen Planus ; Risk Factors
Language	English
Publishing date	2023-01-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.1103533
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Article: Morphea: The 2023 update.

Papara, Cristian / De Luca, David A / Bieber, Katja / Vorobyev, Artem / Ludwig, Ralf J

Frontiers in medicine

2023 Volume 10, Page(s) 1108623

Abstract: Morphea, also known as localized scleroderma, is a chronic inflammatory connective tissue disorder with variable clinical presentations, that affects both adults and children. It is characterized by inflammation and fibrosis of the skin and underlying ... ...

Abstract	Morphea, also known as localized scleroderma, is a chronic inflammatory connective tissue disorder with variable clinical presentations, that affects both adults and children. It is characterized by inflammation and fibrosis of the skin and underlying soft tissue, in certain cases even of the surrounding structures such as fascia, muscle, bone and central nervous system. While the etiology is still unknown, many factors may contribute to disease development, including genetic predisposition, vascular dysregulation, T
Language	English
Publishing date	2023-02-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2023.1108623
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Article ; Online: Protocol to Induce Follicular T Helper Cells, Germinal Centers, and Skin Lesions in Mouse Models for Skin Blistering Diseases.

Bahreini, Farbod / Niebuhr, Markus / Belde, Julia / Bieber, Katja / Westermann, Jürgen / Kalies, Kathrin

Bio-protocol

2022 Volume 12, Issue 10, Page(s) e4414

Abstract: Autoreactive T cells in autoantibody-mediated autoimmune diseases can be divided into two major subsets: (i) follicular T helper cells (Tfh) that provide T cell help in germinal centers (GC) and (ii) effector T (Teff) cells that immigrate into peripheral ...

Abstract	Autoreactive T cells in autoantibody-mediated autoimmune diseases can be divided into two major subsets: (i) follicular T helper cells (Tfh) that provide T cell help in germinal centers (GC) and (ii) effector T (Teff) cells that immigrate into peripheral tissue sites such as the skin and mediate local inflammation. To study the sequence of events leading to the loss of tolerance in autoantibody-mediated autoimmune diseases it is required to investigate both T cell subsets simultaneously. This approach is hampered mainly because the appearance of skin inflammation in mouse models is a random process, which makes it difficult to define the location of inflammation at the right time point. To overcome this problem, we developed a scratching technique for ear skins that leads to the establishment of chronic autoimmune wounds in the mouse model for the pemphigoid-like disease epidermolysis bullosa acquisita. By defining the exact place where the skin wounds should form, this protocol enables a detailed analysis of skin-immigrating Teff cells. Of note, this protocol induces GC in draining lymph nodes in parallel so that Tfh cells in GC can be investigated concurrently. This protocol is not restricted to T cells and can be used for any other skin-immigrating inflammatory cells.
Language	English
Publishing date	2022-05-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4414
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Article ; Online: The complement receptor C5aR2 regulates neutrophil activation and function contributing to neutrophil-driven epidermolysis bullosa acquisita.

Seiler, Daniel L / Kähler, Katja H / Kleingarn, Marie / Sadik, Christian D / Bieber, Katja / Köhl, Jörg / Ludwig, Ralf J / Karsten, Christian M

Frontiers in immunology

2023 Volume 14, Page(s) 1197709

Abstract: Introduction: The function of the second receptor for the complement cleavage product C5a, C5aR2, is poorly understood and often neglected in the immunological context. Using mice with a global deficiency of : Methods: LysM-specific deletion of : ... ...

Abstract	Introduction: The function of the second receptor for the complement cleavage product C5a, C5aR2, is poorly understood and often neglected in the immunological context. Using mice with a global deficiency of Methods: LysM-specific deletion of Results: We confirm the successful deletion of C5aR2 at both the genetic and protein levels in neutrophils. The mice appeared healthy and the expression of C5aR1 in bone marrow and blood neutrophils was not negatively affected by LysM-specific deletion of C5aR2. Using the antibody transfer mouse model of EBA, we found that the absence of Discussion: Overall, with the data presented here, we confirm and extend our previous findings and show that C5aR2 in neutrophils regulates their activation and function in response to C5a by potentially affecting the expression of Fcγ receptors and CD11b. Thus, C5aR2 regulates the finely tuned interaction network between immune complexes, Fcγ receptors, CD11b, and C5aR1 that is important for neutrophil recruitment and sustained activation. This underscores the importance of C5aR2 in the pathogenesis of neutrophil-mediated autoimmune diseases.
MeSH term(s)	Animals ; Mice ; Autoimmune Diseases ; Complement C5a/metabolism ; Epidermolysis Bullosa Acquisita ; Neutrophil Activation ; Neutrophils ; Receptor, Anaphylatoxin C5a/genetics ; Receptor, Anaphylatoxin C5a/metabolism ; Receptors, Complement/metabolism ; Receptors, IgG/metabolism
Chemical Substances	C5ar2 protein, mouse ; Complement C5a (80295-54-1) ; Receptor, Anaphylatoxin C5a ; Receptors, Complement ; Receptors, IgG
Language	English
Publishing date	2023-05-19
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1197709
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Article: Lichen sclerosus: The 2023 update.

De Luca, David A / Papara, Cristian / Vorobyev, Artem / Staiger, Hernán / Bieber, Katja / Thaçi, Diamant / Ludwig, Ralf J

Frontiers in medicine

2023 Volume 10, Page(s) 1106318

Abstract: Lichen sclerosus (LS) is an underdiagnosed inflammatory mucocutaneous condition affecting the anogenital areas. Postmenopausal women are predominantly affected and, to a lesser extent, men, prepubertal children, and adolescents. The etiology of LS is ... ...

Abstract	Lichen sclerosus (LS) is an underdiagnosed inflammatory mucocutaneous condition affecting the anogenital areas. Postmenopausal women are predominantly affected and, to a lesser extent, men, prepubertal children, and adolescents. The etiology of LS is still unknown. Hormonal status, frequent trauma and autoimmune diseases are well-known associations for LS, yet infections do not seem to be clear risk factors. LS pathogenesis involves factors such as a genetic predisposition and an immune-mediated Th1-specific IFNγ-induced phenotype. Furthermore, there is a distinct expression of tissue remodeling associated genes as well as microRNAs. Oxidative stress with lipid and DNA peroxidation provides an enabling microenvironment to autoimmunity and carcinogenesis. Circulating IgG autoantibodies against the extracellular matrix protein 1 and hemidesmosome may contribute to the progression of LS or simply represent an epiphenomenon. The typical clinical picture includes chronic whitish atrophic patches along with itching and soreness in the vulvar, perianal and penile regions. In addition to genital scarring, and sexual and urinary dysfunction, LS may also lead to squamous cell carcinoma. Disseminated extragenital LS and oral LS are also reported. The diagnosis is usually clinical; however, a skin biopsy should be performed in case of an unclear clinical picture, treatment failure or suspicion of a neoplasm. The gold-standard therapy is the long-term application of ultrapotent or potent topical corticosteroids and, alternatively, topical calcineurin inhibitors such as pimecrolimus or tacrolimus. Collectively, LS is a common dermatological disease with a so far incompletely understood pathogenesis and only limited treatment options. To foster translational research in LS, we provide here an update on its clinical features, pathogenesis, diagnosis and (emerging) treatment options.
Language	English
Publishing date	2023-02-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2775999-4
ISSN	2296-858X
ISSN	2296-858X
DOI	10.3389/fmed.2023.1106318
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Article ; Online: Luteolin peracetate and gossypolone inhibit immune complex-mediated neutrophil activation

Yang, Kai / Yin, Junping / Yue, Xiaoyang / Bieber, Katja / Riemekasten, Gabriela / Ludwig, Ralf J / Petersen, Frank / Yu, Xinhua

Frontiers in immunology

2023 Volume 14, Page(s) 1196116

Abstract: Introduction: Natural products have been shown to an important source of therapeutics for human disease. In this study, we aimed to identify natural compounds as potential therapeutics for epidermolysis bullosa acquisita (EBA), an autoimmune disease ... ...

Abstract	Introduction: Natural products have been shown to an important source of therapeutics for human disease. In this study, we aimed to identify natural compounds as potential therapeutics for epidermolysis bullosa acquisita (EBA), an autoimmune disease caused by autoantibodies to type VII collagen (COL7). Methods: Utilizing an Results: Three natural compounds, namely luteolin peracetate, gossypol, and gossypolone were capable in inhibiting the IC-induced neutrophil adhesion and oxygen burst Discussion: In summary, this study demonstrates that luteolin peracetate and gossypolone are potential therapeutics for experimental EBA, which deserves further investigation.
MeSH term(s)	Humans ; Gossypol ; Antigen-Antibody Complex ; Epidermolysis Bullosa Acquisita/drug therapy ; Luteolin ; Neutrophil Activation ; Biological Products ; Immunoglobulin G
Chemical Substances	gossypolone (4547-72-2) ; Gossypol (KAV15B369O) ; Antigen-Antibody Complex ; Luteolin (KUX1ZNC9J2) ; Biological Products ; Immunoglobulin G
Language	English
Publishing date	2023-09-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1196116
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