Related Experiment Video
Updated: Jun 22, 2026

10:27
Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
Published on: December 15, 2011
[Dermatitis herpetiformis. An update of the pathogenesis]
1Klinik und Poliklinik für Dermatologie und Allergologie, Ludwig-Maximilans-Universität München, Frauenlobstr. 9-11, 80337 München. miklos.sardy@med.uni-muenchen.de
Summary
Dermatitis herpetiformis is a skin condition caused by genetics, gluten, and immune system issues. Understanding these factors helps explain how skin symptoms develop.
Area of Science:
- Immunodermatology
- Gastroenterology
- Genetics
Context:
- Dermatitis herpetiformis (DH) is a chronic autoimmune blistering skin disease.
- DH is strongly associated with celiac disease, sharing a common genetic and immunopathogenic basis.
- Current understanding of DH pathogenesis involves a complex interplay of genetic predisposition, environmental triggers, and immune dysregulation.
Purpose:
- To review the multifactorial pathogenesis of dermatitis herpetiformis.
- To synthesize current experimental data on genetic, environmental, and immunological factors.
- To detail the pathophysiological mechanisms leading to skin manifestations in DH.
Summary:
- Genetic background, gluten ingestion, and aberrant immune/autoimmune responses are key pathogenetic factors in DH.
- Other contributing agents and their roles in disease development are also considered.
- Predisposing, inducing factors, and the step-by-step pathophysiological processes culminating in skin symptoms are elucidated.
Impact:
- Provides a comprehensive overview of DH pathogenesis for researchers and clinicians.
- Highlights the critical roles of gluten and immune system dysfunction.
- Facilitates a deeper understanding of DH, potentially informing future therapeutic strategies.
Related Concept Videos
Gastritis-II: Pathophysiology
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology
The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Inflammatory Bowel Disease III: Crohn's Disease
Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Type I Diabetes II: Pathophysiology
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Herpes
Herpes simplex type 1 (HSV‑1) is a widespread pathogen responsible for orolabial lesions. It is an enveloped, double-stranded DNA (dsDNA) virus belonging to the family Herpesviridae. Once the virus infects a host cell, its double‑stranded DNA genome is delivered into the nucleus, where a coordinated cascade of immediate‑early, early, and late gene expression directs viral DNA replication, structural protein synthesis, and virion assembly. After primary infection of epithelial cells, HSV-1...
Genital Herpes
Genital herpes is a sexually transmitted infection primarily caused by herpes simplex virus type 2 (HSV-2), though herpes simplex virus type 1 (HSV-1) is increasingly implicated in genital infections, particularly among younger populations. Transmission occurs mainly through sexual contact, with asymptomatic viral shedding serving as a major route of spread. This characteristic makes HSV-2 difficult to control at a population level, as individuals may unknowingly transmit the virus even in the...
