Autoimmune Bullous Skin Diseases

CD19xCD3 bispecific T cell engager treatment induces remission in experimental pemphigoid disease

The paper tests a CD19xCD3 bispecific T cell engager in a mouse model of pemphigoid disease and finds it induces remission in 45% of treated mice.

Network Toxicology, Molecular Docking, and Molecular Dynamics Simulations Reveal the Mechanism of Tetrabromobisphenol A in Bullous Pemphigoid.

This study identifies molecular mechanisms by which TBBPA contributes to BP pathogenesis using network toxicology, molecular docking, and MD simulations, revealing key targets and interactions.

A human immune system mouse model for preclinical evaluation of therapies in pemphigoid disease

This study develops a human immune system mouse model for EBA, demonstrating that PDK1 inhibition reduces skin inflammation and immune cell activation.

Gut Microbiota Modulates and Predicts Disease Severity in Experimental Pemphigoid Disease

This study shows gut microbiota influences disease severity in an experimental pemphigoid model, with specific taxa linked to protection or inflammation.

IgG autoantibodies in bullous pemphigoid directly induce a pathogenic MyD88-dependent pro-inflammatory response in keratinocytes:

This study shows that BP-IgG autoantibodies induce a pro-inflammatory response in keratinocytes via MyD88-dependent signaling, contributing to BP pathology.

Data-Driven Image Analysis to Determine Antibody-Induced Dissociation of Cell-Cell Adhesion and Antibody Pathogenicity in Pemphigus Vulgaris

This paper introduces a data-driven image analysis approach to quantify antibody-induced changes in cell-cell adhesion and pathogenicity in pemphigus vulgaris.

Desmosomal Cadherin Tension Loss in Pemphigus Vulgaris Mediated by the Inhibition of Active RhoA at Cell-Cell Adhesions

This study shows that PV antibodies cause tension loss at desmosomes and cell-cell adhesions by inhibiting RhoA, which can be partially reversed by altering actomyosin contractility.

In pemphigus, cell detachment, but not autoantibody binding, induces cell-wide, long-lasting transcriptomic and proteomic changes

The paper shows that in pemphigus, cell detachment, not autoantibody binding, causes long-term transcriptomic and proteomic changes associated with blister formation.

Single cell transcriptome profiling reveals pathogenesis of Bullous Pemphigoid

This study uses single-cell transcriptomics to identify functional changes in skin and blood cells during Bullous Pemphigoid, revealing key pathways and cell interactions involved in disease progression.

Pemphigus vulgaris autoantibodies induce an ER stress response

This study shows that PV autoantibodies trigger ER stress, leading to desmosome disruption and cell adhesion loss, and suggests ER stress as a therapeutic target.

Single-Cell Transcriptomes and Immune Repertoires Reveal the Cell State and Molecular Changes in Pemphigus Vulgaris

This study uses single-cell RNA sequencing and immune repertoire analysis to identify key immune cell subtypes and molecular changes in pemphigus vulgaris and assess the impact of prednisone treatment.

Anti-BP180 Autoantibodies Are Present in Stroke and Recognize Human Cutaneous BP180 and BP180-NC16A

The paper investigates the presence of anti-BP180 autoantibodies in stroke patients and finds a higher frequency compared to controls, suggesting a shared autoantigen in stroke and bullous pemphigoid.