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

Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Endocarditis II: Clinical Features of Infective Endocarditis01:25

Endocarditis II: Clinical Features of Infective Endocarditis

Endocarditis can present various clinical features depending on the causative organism and the patient's underlying health conditions. Initially, the clinical features of infective endocarditis develop gradually, presenting with nonspecific symptoms that can be easily mistaken for other illnesses.General SymptomsEarly symptoms of infective endocarditis are fever, chills, weakness, malaise, fatigue, and weight loss. These symptoms reflect the systemic nature of the infection and the body's...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...
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...
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by transmural...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...

You might also read

Related Articles

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

Sort by
Same author

KCNQ1 rs163184 Variant Modulates Susceptibility to Classic and DPP-4 Inhibitor-Associated Bullous Pemphigoid.

International journal of dermatology·2026
Same author

Response to Zou et al, "Comment on "Clinical features, treatment outcomes, and immunologic profile of immune checkpoint inhibitor-associated bullous pemphigoid: A retrospective multicenter cohort study"".

Journal of the American Academy of Dermatology·2026
Same author

International development of Investigator Global Assessment scores for pemphigus.

Journal of the European Academy of Dermatology and Venereology : JEADV·2026
Same author

Clinical features, treatment outcomes, and immunologic profile of immune checkpoint inhibitor-associated bullous pemphigoid: A retrospective multicenter cohort study.

Journal of the American Academy of Dermatology·2026
Same author

Labial adhesions as a rare mucosal manifestation of bullous lupus erythematosus in a 15-year-old female.

International journal of women's dermatology·2026
Same author

Dermoscopy of Subungual Squamous Cell Carcinoma: A Systematic Review.

Cancers·2026

Related Experiment Video

Updated: May 27, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
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

Interstitial granulomatous dermatitis: another clinical variant.

Aikaterini Patsatsi1, Aikaterini Kyriakou, Eva Triantafyllidou

  • 12nd Dermatology Department, Aristotle University School of Medicine, Papageorgiou Hospital, Thessaloniki, Greece.

Case Reports in Dermatology
|November 17, 2011
PubMed
Summary

A rare skin reaction, interstitial granulomatous dermatitis, occurred after stopping adalimumab treatment for rheumatoid arthritis. Lesions resolved upon restarting the medication, suggesting a drug-related cause.

Keywords:
AdalimumabInterstitial granulomatous dermatitisRheumatoid arthritis

Related Experiment Videos

Last Updated: May 27, 2026

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
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

Area of Science:

  • Dermatology
  • Rheumatology
  • Pathology

Background:

  • Adalimumab is a TNF-alpha inhibitor used for rheumatoid arthritis.
  • Interstitial granulomatous dermatitis (IGD) is a histopathological pattern associated with drugs, autoimmune diseases, or rheumatoid arthritis.

Observation:

  • A 70-year-old female patient developed symmetrically distributed erythematous papules around the umbilicus one month after discontinuing adalimumab for rheumatoid arthritis.
  • Skin biopsy revealed an interstitial granulomatous infiltrate without mucin deposition.

Findings:

  • The patient's skin lesions resolved after adalimumab re-initiation, indicating a probable drug-induced etiology.
  • This case presents a distinct clinical manifestation of IGD with symmetrical papules and a mild granulomatous reaction pattern.

Implications:

  • This case highlights a potential adverse cutaneous drug reaction to adalimumab.
  • It underscores the importance of considering drug-induced IGD in patients with rheumatoid arthritis presenting with specific dermatological symptoms.
  • Re-challenging with the suspected drug can aid in diagnosis and management.