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Related Experiment Video

Updated: Jun 27, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

Interleukin 17 sustains rather than induces inflammation.

Francesco Maione¹, Nikolaos Paschalidis, Nicola Mascolo

¹William Harvey Research Institute, Barts and The London School of Medicine, Queen Mary University of London, Charterhouse Square, London EC1M6BQ, UK.

Biochemical Pharmacology

|December 17, 2008

Summary

Interleukin-17 (IL-17) does not initiate inflammation but amplifies existing inflammatory responses. This cytokine selectively recruits neutrophils and boosts pro-inflammatory mediators in pre-inflamed tissues.

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Area of Science:

Immunology
Inflammation Research

Background:

Interleukin-17 (IL-17) is implicated in chronic inflammation and autoimmune diseases.
Research has focused on IL-17-producing cells, with limited investigation into IL-17's direct inflammatory properties.

Purpose of the Study:

To characterize the inflammatory properties of IL-17.
To determine if IL-17 initiates inflammation or exacerbates existing inflammatory conditions.

Main Methods:

Utilized mouse models: hind paw edema and air pouch inflammation.
Administered IL-17 to healthy and pre-inflamed tissues.
Analyzed cellular infiltrates and cytokine/chemokine profiles.

Main Results:

IL-17 injection into healthy hind paws did not induce edema.
IL-17 administration into pre-inflamed air pouches caused sustained inflammation (4-24h).
Induced selective neutrophil (PMN) recruitment and upregulated IL-1beta, IL-6, TNF-alpha, KC, and MCP-1.
Neutralizing anti-KC antibody reduced IL-17's inflammatory effect.

Conclusions:

IL-17 does not initiate inflammatory reactions independently.
IL-17 amplifies biochemical and cellular events in established inflammation.
Chemokine KC plays a significant role in mediating IL-17's inflammatory effects.