Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...
Type I Diabetes II: Pathophysiology01:26

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...
Inflammatory Bowel Disease III: Crohn's Disease01:25

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...
Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Reticulated Erythematous Mucinosis Preceding the Clinical Diagnosis of Hepatitis C Virus-Related Hepatocellular Carcinoma.

The Journal of dermatology·2026
Same author

Bullous Pemphigoid With Blister Sparing in Areas of Neurologic Impairment Caused by Syringomyelia.

The Journal of dermatology·2026
Same author

mTOR-Responsive PIK3CA p.E542K-Harboring Sweat Gland Carcinoma With Neuroendocrine Differentiation.

International journal of dermatology·2026
Same author

Widespread ulcerative genital herpes in a patient with Good syndrome.

Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG·2026
Same author

Prevalence of birch pollinosis and oral allergy syndrome in the general population of Hokkaido, Japan.

Auris, nasus, larynx·2026
Same author

Recurrent cutaneous eosinophilic vasculitis in a child.

European journal of dermatology : EJD·2026

Related Experiment Video

Updated: Jun 1, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Pathogenesis of bullous pemphigoid.

Hideyuki Ujiie1, Wataru Nishie, Hiroshi Shimizu

  • 1Department of Dermatology, Hokkaido University Graduate School of Medicine, N-15 W-7, Kita-ku, Sapporo 060-8638, Japan. h-ujiie@med.hokudai.ac.jp

Dermatologic Clinics
|May 25, 2011
PubMed
Summary

Bullous pemphigoid is an autoimmune blistering disease caused by autoantibodies targeting type XVII collagen. Research shows these antibodies, along with T cells, trigger immune responses leading to disease development.

More Related Videos

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid
05:05

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid

Published on: June 17, 2025

Related Experiment Videos

Last Updated: Jun 1, 2026

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid
05:05

Technique of Conjunctival Biopsy and Direct Immunofluorescence for Diagnosing Mucous Membrane Pemphigoid

Published on: June 17, 2025

Area of Science:

  • Immunodermatology
  • Autoimmunity
  • Molecular Biology

Background:

  • Bullous pemphigoid (BP) is the most common autoimmune blistering disease.
  • BP pathogenesis involves autoantibodies against type XVII collagen (COL17A1).
  • Understanding BP mechanisms is crucial for developing targeted therapies.

Purpose of the Study:

  • To elucidate the pathogenic mechanisms of bullous pemphigoid.
  • To investigate the role of autoantibodies and T cells in BP.
  • To explore the contribution of complement activation and cellular infiltration.

Main Methods:

  • Passive transfer of IgG and IgE autoantibodies against COL17A1 in animal models.
  • In vitro studies on COL17A1 ectodomain shedding.
  • Analysis of immune responses including complement activation, mast cell degranulation, and neutrophil/eosinophil infiltration.
  • Evaluation of autoreactive CD4+ T lymphocyte involvement.

Main Results:

  • Passive transfer of anti-COL17A1 antibodies confirmed their pathogenicity.
  • Immune responses observed include complement activation, mast cell degranulation, and inflammatory cell infiltration.
  • In vitro studies provided insights into COL17A1 shedding.
  • Autoreactive CD4+ T lymphocytes play a role in pathogenic autoantibody development.

Conclusions:

  • Autoantibodies against type XVII collagen are key drivers of bullous pemphigoid.
  • Immune responses involving complement, mast cells, and inflammatory cells contribute to BP.
  • CD4+ T cells are important for the development of pathogenic autoantibodies in BP.
  • Further research into these pathways may lead to novel therapeutic strategies.