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Related Experiment Video

Updated: Jun 22, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Cytokines decrease expression of interleukin-6 signal transducer and leptin receptor in central nervous system glia.

Jason J Rose¹, Beverly Bealmear, Liljana Nedelkoska

¹Department of Neurology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

Journal of Neuroscience Research

|May 30, 2009

Summary

Cytokines in the central nervous system (CNS) affect multiple sclerosis (MS) lesion formation. This study found that certain cytokines down-regulate key genes, potentially impacting MS disease progression.

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Published on: January 4, 2018

Area of Science:

Neuroimmunology
Molecular Biology
Cellular Biology

Background:

Cytokines secreted in the CNS modulate multiple sclerosis (MS) lesion formation.
Th1 lymphocytes and monocyte/macrophages (MM) are implicated in lesion induction, while Th2 lymphocytes may inhibit formation.

Purpose of the Study:

To investigate the role of Th1, Th2, and M/M-representative cytokines on gene expression in cultured CNS glia.
To analyze the temporal effects of these cytokines on interleukin-6 (IL-6) signal transducer (IL-6st) and leptin receptor (obr) expression.

Main Methods:

Gene arrays were used to assess gene expression in cultured CNS glia exposed to representative cytokines.
Rat CNS glial cultures were incubated with cytokines for durations ranging from 6 hours to 5 days.
Immunocytochemical staining was employed to visualize IL-6st and leptin receptor expression in glia.

Main Results:

Cytokines increased interleukin-6 (IL-6) gene expression and decreased leptin receptor (obr) expression at 6 hours.
IL-6 signal transducer (IL-6st) expression showed no initial change but was down-regulated over time (up to 5 days) along with leptin receptor.
Both IL-6st and leptin receptor were expressed in multiple glia types, with reduced IL-6st by day 3.

Conclusions:

Cytokine-induced down-regulation of IL-6st and leptin receptor in glia may reduce pro-inflammatory IL-6 signaling.
This down-regulation could also impair responses to regenerative growth factors, potentially influencing the course of MS.
Understanding these molecular mechanisms is crucial for developing therapeutic strategies for MS.