Related Experiment Video

Updated: Jul 28, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

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

TNF-alpha suppresses CR3-mediated myelin removal by macrophages

W Brück1, Y Brück, R L Friede

  • 1Department of Neuropathology, University of Göttingen, Germany.

Journal of Neuroimmunology
|May 1, 1992
PubMed

Insights

Tumor necrosis factor-alpha (TNF-alpha) significantly impairs myelin ingestion by macrophages during Wallerian degeneration by reducing complement receptor type 3 (CR3) expression. Interleukin-1 showed no effect in this in vitro study.

Area of Science:

  • Neuroimmunology
  • Cellular Biology
  • Myelin Biology

Background:

  • Mononuclear cells, particularly macrophages, are crucial for clearing myelin debris following nerve injury (Wallerian degeneration).
  • Macrophage-mediated myelinophagy is a key process in nerve regeneration.
  • Cytokines secreted by macrophages can modulate their own function.

Purpose of the Study:

  • To investigate the role of macrophage-secreted cytokines, specifically tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1), in myelin ingestion.
  • To elucidate the mechanism by which TNF-alpha affects myelin clearance by macrophages.

Main Methods:

  • In vitro study using macrophages and myelin.
  • Treatment with TNF-alpha and IL-1.
  • Assessment of myelin ingestion via complement receptor type 3 (CR3).
  • Immunofluorescence to analyze CR3 expression on macrophages.
  • Investigation of TNF-alpha receptor interaction.

Main Results:

  • TNF-alpha treatment significantly reduced myelin ingestion by macrophages.
  • This reduction was mediated by decreased expression of CR3 on phagocytic cells.
  • Anti-TNF-alpha antibodies restored normal myelin ingestion levels.
  • IL-1 had no significant effect on myelin ingestion in this experimental system.
  • Evidence of TNF-alpha interacting with its receptor on the macrophage cell membrane was observed.

Conclusions:

  • TNF-alpha plays an inhibitory role in macrophage-mediated myelin clearance during Wallerian degeneration.
  • The mechanism involves down-regulation of complement receptor type 3 (CR3) expression.
  • Targeting TNF-alpha may offer therapeutic potential for enhancing myelin debris clearance and promoting nerve repair.

More Related Videos

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes11:48

Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes

Published on: May 31, 2018

Highly Efficient Transfection of Primary Macrophages with In Vitro Transcribed mRNA06:46

Highly Efficient Transfection of Primary Macrophages with In Vitro Transcribed mRNA

Published on: November 9, 2019

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
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...