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Updated: Jun 24, 2026

Artificial Antigen Presenting Cell (aAPC) Mediated Activation and Expansion of Natural Killer T Cells
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Published on: December 29, 2012

The cyclic AMP response element modulator {alpha} suppresses CD86 expression and APC function.

Martina Ahlmann1, Georg Varga, Karsten Sturm

  • 1Institute of Immunology, University of Münster, Germany.

Journal of Immunology (Baltimore, Md. : 1950)
|March 21, 2009
PubMed
Summary
This summary is machine-generated.

The cAMP response element modulator (CREM)alpha acts as a key repressor in T cell immunity. Suppressing CREMalpha boosts T cell proliferation and costimulation, impacting immune responses.

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Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • The cAMP response element modulator (CREM)alpha is a transcriptional repressor involved in T cell immune response termination.
  • Abnormal T cell function in systemic lupus erythematosus is linked to CREMalpha.
  • Understanding CREMalpha's role in antigen-presenting cells (APCs) is crucial for immune regulation.

Purpose of the Study:

  • To investigate the role of CREMalpha in regulating APC function and T cell proliferation.
  • To determine if CREMalpha directly impacts the expression of costimulatory molecules like CD86.
  • To assess the in vivo consequences of altered CREMalpha activity on T cell-mediated immune responses.

Main Methods:

  • Analysis of CD86 expression in APCs from Crem(-/-) mice and human APCs with suppressed CREMalpha.
  • Chromatin immunoprecipitation assays to assess CREMalpha binding to the CD86 promoter.
  • In vitro T cell proliferation assays (antigen-dependent and independent).
  • In vivo contact dermatitis models using APCs from Crem(-/-) and Crem(+/+) mice.

Main Results:

  • APCs from Crem(-/-) mice exhibited increased CD86 expression and enhanced T cell proliferation.
  • Selective suppression of CREMalpha in human APCs led to higher surface CD86 levels.
  • CREMalpha was shown to bind the CD86 promoter and repress its activity.
  • Transfer of Crem(-/-) APCs induced a stronger contact dermatitis response in vivo.

Conclusions:

  • CREMalpha functions as a critical negative regulator of costimulation.
  • CREMalpha plays a significant role in controlling APC-dependent T cell function.
  • These findings highlight CREMalpha as a potential therapeutic target for modulating T cell immunity.