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Updated: Jul 8, 2026

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries
08:49

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

Published on: January 22, 2019

[The signaling mechanism of glucocorticoid-induced T-cell apoptosis]

Taijiro Okabe1, Ryouichi Takayanagi, Toshihiko Yanase

  • 1Department of Medicine and Bioregulatory Science, Graduate School of Medical Science, Kyushu University.

Nihon Rinsho. Japanese Journal of Clinical Medicine
|January 15, 2008
PubMed

Insights

Glucocorticoid resistance in T-cells may be overcome by targeting extracellular signal-regulated protein kinase (ERK). This kinase inhibits programmed cell death, offering potential therapeutic strategies for glucocorticoid-resistant conditions.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Context:

  • Glucocorticoids are widely used to treat inflammatory and autoimmune diseases.
  • Glucocorticoid-induced T-cell apoptosis is a key mechanism of action.
  • Understanding the molecular pathways regulating this process is crucial for improving therapeutic efficacy.

Purpose:

  • To investigate the role of extracellular signal-regulated protein kinase (ERK) in glucocorticoid-induced T-cell apoptosis.
  • To identify potential molecular targets for overcoming glucocorticoid resistance.

Summary:

  • Glucocorticoid-induced T-cell apoptosis is generally believed to involve alterations in gene expression, with increased proapoptotic or decreased antiapoptotic gene activity.
  • However, the specific target genes remain unidentified.
  • Recent findings indicate that extracellular signal-regulated protein kinase (ERK) actively inhibits glucocorticoid-induced T-cell apoptosis.

Impact:

  • The identification of ERK as an inhibitor of glucocorticoid-induced T-cell apoptosis provides a novel target.
  • This discovery may lead to the development of new therapeutic strategies to overcome glucocorticoid resistance in T-cell mediated diseases.

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