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Serum interleukin-10 level is increased and correlated positively with disease severity in patients with dipeptidyl peptidase-4 inhibitor-related bullous pemphigoid.
J Dermatol
January 2025
Department of Dermatology, Teikyo University School of Medicine, Tokyo, Japan.
Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease with a linear deposit of autoantibodies at the epidermal basement membrane zone. It was reported that diabetes patients who took a dipeptidyl peptidase-4 inhibitor (DPP4i), an oral antidiabetic drug, had an increased incidence of BP. However, data on DPP4i-related BP are limited.
View Article and Find Full Text PDFPathophysiology of Bullous Pemphigoid: Role of Type 2 Inflammation and Emerging Treatment Strategies (Narrative Review).
Adv Ther
December 2024
Sanofi, Cambridge, MA, USA.
Article Synopsis
- Bullous pemphigoid (BP) is an autoimmune blistering disease mainly seen in older adults, significantly affecting their quality of life.
- The disease involves autoantibodies against specific proteins and displays characteristics of type 2 inflammation, including high levels of IgE and eosinophils, along with increased type 2 cytokines in skin lesions.
- This review highlights the pathophysiology of BP, the impact of biologics targeting type 2 immune mediators, and the potential for future targeted therapies to improve treatment options.
Type XVII Collagen-Specific CD4 T Cells Induce Bullous Pemphigoid by Producing IL-5.
J Invest Dermatol
September 2024
Department of Dermatology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. Electronic address:
Article Synopsis
- Bullous pemphigoid is an autoimmune skin disease caused by antibodies against type XVII collagen, leading to blister formation and inflammation in the skin.
- Researchers created specific CD4 T cell lines that recognize the collagen and tested their effects by transferring them into specially designed mice that only express human COL17.
- The study found that certain T cell lines caused symptoms similar to bullous pemphigoid, and high levels of IL-5 cytokine were linked to this effect; blocking IL-5 reduced the skin damage and antibody production.
Single-cell transcriptomics analysis of bullous pemphigoid unveils immune-stromal crosstalk in type 2 inflammatory disease.
Nat Commun
July 2024
Hospital for Skin Diseases, Shandong First Medical University, Jinan, Shandong, China.
Bullous pemphigoid (BP) is a type 2 inflammation- and immunity-driven skin disease, yet a comprehensive understanding of the immune landscape, particularly immune-stromal crosstalk in BP, remains elusive. Herein, using single-cell RNA sequencing (scRNA-seq) and in vitro functional analyzes, we pinpoint Th2 cells, dendritic cells (DCs), and fibroblasts as crucial cell populations. The IL13-IL13RA1 ligand-receptor pair is identified as the most significant mediator of immune-stromal crosstalk in BP.
View Article and Find Full Text PDFRadiofrequency Treatment Attenuates Age-Related Changes in Dermal-Epidermal Junctions of Animal Skin.
Int J Mol Sci
May 2024
Department of Anatomy & Cell Biology, College of Medicine, Gachon University, Incheon 21936, Republic of Korea.
The dermal-epidermal junction (DEJ) is essential for maintaining skin structural integrity and regulating cell survival and proliferation. Thus, DEJ rejuvenation is key for skin revitalization, particularly in age-related DEJ deterioration. Radiofrequency (RF) treatment, known for its ability to enhance collagen fiber production through thermal mechanisms and increase heat shock protein (HSP) expression, has emerged as a promising method for skin rejuvenation.
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