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Inflammation

Inflammation

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...

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,...

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...

Acute Inflammation I: Inflammatory Response

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect...

Acute Inflammation I: Cellular Phase

Acute Inflammation I: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...

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Related Experiment Video

Updated: May 5, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 27, 2013

The IL-23/IL-17 axis in inflammation.

Yoichiro Iwakura¹, Harumichi Ishigame

¹Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan. iwakura@ims.u-Tokyo.ac.jp

The Journal of Clinical Investigation

|May 4, 2006

Summary

Blocking the IL-23/IL-17 pathway, not IL-12, suppresses inflammatory diseases like IBD and MS in animal models. This highlights IL-23 and IL-17 as potential therapeutic targets for chronic inflammatory conditions.

Area of Science:

Immunology
Cellular Biology
Inflammation Research

Background:

Interleukin-23 (IL-23) drives the differentiation of CD4(+) T cells into pathogenic Th17 cells.
Th17 cells produce cytokines including IL-17, IL-17F, IL-6, and TNF-alpha, which are implicated in inflammatory processes.
IFN-gamma and IL-4 are not produced by these Th17 cells.

Purpose of the Study:

To investigate the role of the IL-23/IL-17 pathway in the development of inflammatory diseases.
To evaluate the therapeutic potential of blocking IL-23, IL-17, or IL-6 in relevant animal models.
To compare the efficacy of targeting the IL-23/IL-17 pathway versus the IL-12/IFN-gamma pathway.

Main Methods:

Utilized animal models of inflammatory bowel disease (IBD) and multiple sclerosis (MS).

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Last Updated: May 5, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

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Administered blocking agents targeting IL-23, IL-17, IL-6, or IL-12/IFN-gamma pathways.

Assessed the suppression of disease development in response to targeted interventions.

Main Results:

Blocking IL-23 significantly suppressed disease progression in animal models.
Inhibition of downstream factors IL-17 and IL-6 also demonstrated significant disease suppression.
Targeting the IL-12/IFN-gamma pathway did not effectively suppress disease development.

Conclusions:

The IL-23/IL-17 pathway plays a critical role in the pathogenesis of chronic inflammatory diseases.
Blocking IL-23 or its downstream cytokines IL-17 and IL-6 represents a promising therapeutic strategy.
These findings suggest novel therapeutic targets for treating inflammatory bowel disease and multiple sclerosis.