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Related Experiment Video

Updated: May 28, 2026

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse

In Vitro Differentiation of Naive CD4⁺ T Cells into Pathogenic Th17 Cells in Mouse

Published on: October 25, 2024

Platelet-activating factor induces Th17 cell differentiation.

Anne-Marie Drolet¹, Maryse Thivierge, Sylvie Turcotte

¹Immunology Division, Department of Pediatrics, Faculty of Medicine and Health Sciences, Université de Sherbrooke, Sherbrooke, QC, Canada J1H 5N4.

Mediators of Inflammation

|October 21, 2011

Summary

This summary is machine-generated.

Platelet-activating factor (PAF) promotes the development of T helper 17 (Th17) cells, which are involved in autoimmune diseases. This finding suggests new therapeutic targets for inflammatory conditions.

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Area of Science:

Immunology
Cell Biology

Background:

T helper 17 (Th17) cells are implicated in inflammatory and autoimmune diseases.
Platelet-activating factor (PAF) is a phospholipid mediator found in inflammatory lesions, known to induce IL-6 production.

Purpose of the Study:

To investigate the effect of PAF on Th17 cell development.
To explore the role of PAF in initiating inflammatory processes.

Main Methods:

Monocyte-derived Langerhans cells (LCs) and keratinocytes were treated with PAF.
T cells were co-cultured with PAF-pretreated LCs and stimulated.
Expression of Th17-related genes and proteins was analyzed.
PAF receptor antagonist (WEB2086) and neutralizing antibodies (anti-IL-23, anti-IL-6R) were used to block PAF signaling.

Main Results:

Picomolar PAF induced IL-23, IL-6, and IL-1β expression in LCs and keratinocytes.
PAF pretreatment of LCs promoted Th17 cell differentiation, increasing RORγt, IL-17, IL-21, and IL-22 expression.
PAF-induced Th17 development was inhibited by WEB2086, anti-IL-23, and anti-IL-6R.

Conclusions:

PAF acts as a novel stimulus for Th17 cell development.
This pathway represents a potential therapeutic target for inflammatory and autoimmune diseases.