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Related Experiment Videos

CD28 signals through acidic sphingomyelinase

L M Boucher1, K Wiegmann, A Fütterer

  • 1Institute of Medical Microbiology, Technical University of Munich, Germany.

The Journal of Experimental Medicine
|June 1, 1995
PubMed
Summary
This summary is machine-generated.

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Costimulatory molecule CD28 activates acidic sphingomyelinase (A-SMase), generating ceramide. This pathway is crucial for T cell activation, highlighting a novel signaling mechanism for T lymphocyte responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • T cell activation requires antigen recognition plus costimulatory signals.
  • Costimulatory molecule CD28 plays a critical role in T cell responses.
  • The intracellular signaling pathways downstream of CD28 are not fully understood.

Purpose of the Study:

  • To investigate the novel intracellular signaling pathway initiated by the costimulatory molecule CD28.
  • To elucidate the role of acidic sphingomyelinase (A-SMase) in CD28-mediated costimulation.

Main Methods:

  • Investigated CD28 engagement in primary T cells and Jurkat T cells.
  • Assessed acidic sphingomyelinase (A-SMase) activation and ceramide generation.
  • Utilized overexpression of recombinant A-SMase in Jurkat T cells.

Related Experiment Videos

Main Results:

  • CD28 engagement triggers the activation of acidic sphingomyelinase (A-SMase).
  • A-SMase activation leads to the generation of ceramide, a lipid messenger.
  • A-SMase activation by CD28 was observed in both resting and activated T cells.
  • Ligation of CD3 or CD2 did not activate A-SMase.
  • Overexpression of A-SMase mimicked CD28's effect on nuclear factor-kB activation.

Conclusions:

  • CD28 provides a critical costimulatory signal through the activation of the acidic sphingomyelinase (A-SMase) pathway.
  • This pathway generates ceramide, influencing T cell activation and nuclear factor-kB activity.
  • The findings reveal a novel mechanism by which CD28 regulates T lymphocyte responses.