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

T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
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 IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...

You might also read

Related Articles

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

Sort by
Same author

Surgical Technique and Oro-Nasal Fistula Formation After Primary Palatoplasty: A Comparative Study of Closed Intravelar and Modified Veau-Wardill-Kilner Techniques.

Journal of clinical medicine·2026
Same author

Vascular Proliferation in Biopsies from Active Lichen Planopilaris as a Novel Pathologic Finding.

The American Journal of dermatopathology·2026
Same author

Exploring the Potential Link Between Minoxidil Use and Rosacea Using A Real-World Data Base.

Journal of drugs in dermatology : JDD·2026
Same author

Biopsy from the epicenter of the scalp whorl diagnoses early lichen planopilaris.

Journal of the American Academy of Dermatology·2025
Same author

Anagen Effluvium: A Rare Side Effect After Radiation Therapy for Auricular Keloids.

Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]·2025
Same author

Frontal fibrosing alopecia part I - Diagnosis and clinical presentation.

Journal of the American Academy of Dermatology·2025

Related Experiment Videos

Psoriasis: targeting therapy towards the inflammatory cascade.

Mariya Miteva1

  • 1Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL, USA. mmiteva@med.miami.edu

American Journal of Clinical Dermatology
|July 1, 2010
PubMed
Summary

Psoriasis is a chronic inflammatory skin and joint disease. Tumor necrosis factor alpha (TNFalpha) is key in its inflammation, and blocking it with therapies like biologics is effective.

Related Experiment Videos

Area of Science:

  • Immunodermatology
  • Inflammatory Diseases

Background:

  • Psoriasis is a chronic relapsing/remitting inflammatory condition affecting skin and joints.
  • While T-cells are central, epidermal keratinocyte alterations are also significant in psoriasis pathogenesis.
  • Tumor necrosis factor alpha (TNFalpha) is a critical cytokine in the psoriatic inflammatory cascade.

Purpose of the Study:

  • To highlight the role of TNFalpha in psoriasis.
  • To underscore the therapeutic potential of targeting TNFalpha.

Main Methods:

  • Review of existing literature on psoriasis pathogenesis.
  • Analysis of the role of cytokines, specifically TNFalpha.
  • Evaluation of therapeutic strategies targeting TNFalpha.

Main Results:

  • Psoriasis involves complex immune dysregulation with keratinocyte involvement.
  • TNFalpha is a pivotal mediator of inflammation in psoriasis.
  • Therapies inhibiting TNFalpha function demonstrate significant clinical efficacy.

Conclusions:

  • Targeting TNFalpha is a validated and effective therapeutic strategy for psoriasis.
  • Understanding the inflammatory cascade, including TNFalpha, is crucial for managing psoriasis.