Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

The JAK-STAT Signaling Pathway

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...

T Cell Types and Functions

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...

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...

Immunoglobulin-like Cell Adhesion Molecules

Immunoglobulin-like Cell Adhesion Molecules

Immunoglobulin-like cell adhesion molecules or Ig-CAMs are a versatile group of cell surface glycoproteins belonging to the immunoglobulin protein superfamily. Ig-CAMs possess the characteristic immunoglobulin protein domains and other domains such as the fibronectin type III domain. The Ig domains are glycosylated to varying degrees in different Ig-CAMs.
Ig-CAMs exhibit either homophilic binding (to other Ig-CAMs) or heterophilic binding (to other ligands such as integrins). While most Ig-CAMs...

Inflammatory Response

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,...

TGF - β Signaling Pathway

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

You might also read

Related Articles

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

Sort by

Same author

IL-33 Exacerbates Periodontal Disease through Induction of RANKL.

Journal of dental research·2015

Same author

Regulation of delayed-type hypersensitivity to pathogens and alloantigens.

Immunology today·2014

Same author

This letter was sent to Dr Liew, who replied as follows.

Immunology today·2014

Same author

IL-33 targeting attenuates intestinal mucositis and enhances effective tumor chemotherapy in mice.

Mucosal immunology·2014

Same author

An interleukin-33/ST2 signaling deficiency reduces overt pain-like behaviors in mice.

Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas·2013

Same author

IL-33/ST2 signalling contributes to carrageenin-induced innate inflammation and inflammatory pain: role of cytokines, endothelin-1 and prostaglandin E2.

British journal of pharmacology·2013

Search research articles

Related Experiment Video

Updated: May 23, 2026

A Strategy for the Study of IL-9-Producing Lymphoid Cells in the Nippostrongylus brasiliensis Infection Model

A Strategy for the Study of IL-9-Producing Lymphoid Cells in the Nippostrongylus brasiliensis Infection Model

Published on: March 3, 2023

IL-33: a Janus cytokine.

¹Institute of Infection, Immunity and Inflammation, University of Glasgow, 120, University Place, Glasgow G12 8TA, UK. foo.liew@glasgow.ac.uk

Annals of the Rheumatic Diseases

|March 31, 2012

Summary

Interleukin 33 (IL-33) enhances host defense against infections like Trichuris and sepsis. However, this immune mediator also exacerbates conditions such as allergies and arthritis, highlighting its dual role.

Area of Science:

Immunology
Molecular Biology
Infectious Diseases

Background:

Interleukin 33 (IL-33) is a cytokine belonging to the IL-1 family.
IL-33 binds to the ST2 receptor, primarily found on Th2 cells and mast cells.
IL-33 influences T-cell polarization, shifting from Th1 to Th2 phenotypes.

Purpose of the Study:

To investigate the role of IL-33 in host defense mechanisms.
To explore the impact of IL-33 on various inflammatory and infectious conditions.
To evaluate the therapeutic potential and risks associated with IL-33 modulation.

Main Methods:

Analysis of IL-33 gene expression during nematode infection (Trichuris muris).
Assessment of IL-33 treatment effects on resistance to Trichuris infection.

More Related Videos

Induction of Ocular Surface Inflammation and Collection of Involved Tissues

Induction of Ocular Surface Inflammation and Collection of Involved Tissues

Published on: August 4, 2022

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes

Published on: May 31, 2018

Related Experiment Videos

Last Updated: May 23, 2026

A Strategy for the Study of IL-9-Producing Lymphoid Cells in the Nippostrongylus brasiliensis Infection Model

A Strategy for the Study of IL-9-Producing Lymphoid Cells in the Nippostrongylus brasiliensis Infection Model

Published on: March 3, 2023

Induction of Ocular Surface Inflammation and Collection of Involved Tissues

Induction of Ocular Surface Inflammation and Collection of Involved Tissues

Published on: August 4, 2022

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes

Published on: May 31, 2018

Evaluation of IL-33's role in sepsis models and atherosclerosis.

Investigation of IL-33's influence on allergic responses and arthritis.

Main Results:

IL-33 mRNA is upregulated early in Trichuris muris infection.
IL-33 administration enhances resistance to Trichuris infection and attenuates sepsis.
IL-33 reduces atherosclerosis and adipocyte inflammation by inducing type II cytokines.
Conversely, IL-33 exacerbates allergic reactions and arthritis.

Conclusions:

IL-33 plays a conserved role in host defense against infections.
IL-33 exhibits context-dependent effects, acting as a double-edged sword.
Targeting IL-33 requires careful consideration due to its potential to exacerbate certain inflammatory conditions.