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T Cell Types and Functions01:24

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...

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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
09:12

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Published on: January 30, 2014

Ciliary neurotrophic factor and interleukin-6 differentially activate microglia.

J Kyle Krady1, Hsiao-Wen Lin, Christina M Liberto

  • 1Department of Neural and Behavioral Sciences, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.

Journal of Neuroscience Research
|January 25, 2008
PubMed
Summary

Ciliary neurotrophic factor (CNTF) supports neuron survival by modulating microglia, while Interleukin-6 (IL-6) increases microglial neurotoxicity. These distinct effects stem from different intracellular signaling pathways activated by these cytokines following CNS injury.

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Published on: April 13, 2017

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Cytokines released after central nervous system (CNS) injury influence microglial functions, impacting both support and cytotoxicity.
  • Interleukin-6 (IL-6)-family cytokines are among the key factors released during CNS injury, necessitating an understanding of microglial responses.

Purpose of the Study:

  • To investigate the differential effects of ciliary neurotrophic factor (CNTF) and Interleukin-6 (IL-6) on primary rat microglia.
  • To elucidate the functional consequences of microglial activation by CNTF and IL-6 on neuronal survival and inflammatory mediator expression.
  • To explore the underlying intracellular signaling mechanisms (STAT-3 and ERK phosphorylation) responsible for the distinct microglial responses.

Main Methods:

  • Primary rat microglia cultures were stimulated with CNTF and IL-6.
  • Microglial activation was assessed by measuring the expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and cyclooxygenase-2 (COX-2).
  • Trophic factor expression (GDNF) and conditioned media effects on motor neuron survival were evaluated.
  • Intracellular signaling pathways, specifically STAT-3 and ERK phosphorylation, were analyzed following cytokine stimulation.

Main Results:

  • CNTF treatment reduced COX-2 levels and enhanced glial cell-line derived neurotrophic factor (GDNF) mRNA and protein secretion.
  • IL-6 treatment increased the expression of IL-1beta, TNF-alpha, and COX-2, with no effect on GDNF.
  • Conditioned media from CNTF-stimulated microglia significantly promoted motor neuron survival, whereas IL-6-stimulated microglia decreased neuronal survival.
  • IL-6 markedly increased STAT-3 and ERK phosphorylation, while CNTF induced only weak phosphorylation of these signaling molecules.

Conclusions:

  • CNTF promotes microglial activation that supports neuronal survival, contrasting with IL-6, which enhances microglial neurotoxic potential.
  • The opposing effects of CNTF and IL-6 on microglia are mediated by distinct intracellular signaling pathways, particularly STAT-3 and ERK activation.
  • Understanding these differential signaling mechanisms is crucial for developing targeted therapies for CNS injury.