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

1.4K
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...
1.4K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

9.3K
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...
9.3K
Inflammatory Response01:28

Inflammatory Response

8.1K
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,...
8.1K
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

6.5K
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...
6.5K
T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

5.5K
T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
5.5K
Allergic Drug Reactions01:27

Allergic Drug Reactions

983
Allergic reactions related to drugs are hypersensitivity responses driven by the immune system and bear no connection to the drug's therapeutic action. While drugs in isolation do not trigger an immune response, they can interact with endogenous proteins to form antigens. These antigens stimulate lymphocytes to produce antibodies. IgE-type antibodies attach themselves to mast cells. Upon subsequent exposure to the same stimulus, the antigen-antibody interaction is initiated, unleashing...
983

You might also read

Related Articles

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

Sort by
Same author

Real-World Outcomes of Prophylaxis With rIX-FP in Germany: A Prospective, Non-Interventional Study in Haemophilia B.

Haemophilia : the official journal of the World Federation of Hemophilia·2026
Same author

VKORC1L1-mediated vitamin K recycling counters ferroptosis to promote endothelial repair.

Scientific reports·2026
Same author

Management of Breakthrough Bleeding During Emicizumab Prophylaxis in Acquired Haemophilia A: Data From the GTH-AHA-EMI Study.

Haemophilia : the official journal of the World Federation of Hemophilia·2026
Same author

Real-world provider experiences with hemophilia A gene therapy: administration of valoctocogene roxaparvovec.

Research and practice in thrombosis and haemostasis·2026
Same author

Final data from the German AHEAD study: effectiveness and safety of octocog alfa and rurioctocog alfa pegol for hemophilia A in a real-world setting.

Therapeutic advances in hematology·2026
Same author

Gait Pattern at Different Speeds in Persons With Haemophilia.

Haemophilia : the official journal of the World Federation of Hemophilia·2026

Related Experiment Video

Updated: Sep 16, 2025

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System
10:25

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System

Published on: September 20, 2019

7.1K

Langerhans Cell Modulation in Atopic Dermatitis Is TLR2/SOCS1-Dependent and JAK Inhibitor-Sensitive.

Yuxuan Deng1,2, Nicole Leib1, Sylvia Schnautz1

  • 1Center for Skin Diseases, University Hospital Bonn, Bonn, Germany.

Allergy
|July 9, 2025
PubMed
Summary

Langerhans cells (LC) in atopic dermatitis (AD) show desensitization to Toll-like receptor 2 (TLR2) due to Staphylococcus aureus. This desensitization involves SOCS1 and impacts cytokine release, offering insights into AD mechanisms.

Keywords:
JAK/STATLangerhans cellsTLR2atopic dermatitismicrobiome

More Related Videos

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.6K
Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
08:25

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis

Published on: September 26, 2022

2.9K

Related Experiment Videos

Last Updated: Sep 16, 2025

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System
10:25

Assessment of Lymphocyte Migration in an Ex Vivo Transmigration System

Published on: September 20, 2019

7.1K
Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.6K
Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
08:25

Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis

Published on: September 26, 2022

2.9K

Area of Science:

  • Immunology
  • Dermatology
  • Cell Biology

Background:

  • Langerhans cells (LC) are crucial for skin immunity and microbiome sensing via Toll-like receptors (TLR).
  • Impaired LC function is observed in atopic dermatitis (AD), potentially due to persistent Staphylococcus aureus exposure.
  • This study investigates the hypothesis of LC desensitization mediated by TLR2 in AD.

Purpose of the Study:

  • To investigate the desensitization of human LC in response to TLR2 ligands, mimicking AD conditions.
  • To explore the role of TLR2 signaling and its regulators in LC dysfunction.
  • To evaluate the impact of JAK inhibitors on LC responsiveness.

Main Methods:

  • Human LC were generated and desensitized via repetitive TLR2 ligand exposure (priming).
  • TLR responsiveness was assessed using flow cytometry, qPCR, and transwell assays.
  • Expression of maturation/migration markers, cytokine release, and downstream molecules was analyzed.

Main Results:

  • Primed LC exhibited desensitization to TLR2 activation, with impaired expression of CD83, CD80, CD86, and MHCII.
  • Chemokine regulation (CCR6, CCR7), migration, and Th17-driving cytokine production were reduced in primed LC.
  • Elevated IL-18 and IL-1β levels were observed, alongside upregulated negative TLR2 regulators (SOCS1, IRAKM).
  • JAK inhibitors reduced SOCS1 and restored activation markers but did not affect IRAKM.

Conclusions:

  • Primed LC accurately model the impaired TLR2 responsiveness seen in AD.
  • This study reveals a novel contribution of LC to AD-associated IL-1β and IL-18 production.
  • The findings elucidate the mechanistic role of SOCS1 and the action of JAK inhibitors in this context.