lpr T cells have lower ability to maintain bcl-2 expression ex vivo

  • Y. Matsumoto
  • , T. Shinzato
  • , I. Takai
  • , Y. Kimura
  • , S. Nakai
  • , M. Miwa
  • , K. Fuse
  • , Y. Yoshikai
  • , K. Maeda

Research output: Contribution to journalArticlepeer-review

Abstract

Autoimmune-prone lpr mice develop lymphoproliferative disorders, whereas their lymphocytes show accelerated apoptosis in culture. To elucidate whether the bcl-2 protein, a repressor of apoptosis, is critical to the discrepancy between in vivo and in vitro survival, we examined bcl-2 expression in T cells from +/+ and lpr mice during culture. The expression levels of bcl-2 in cultured T cells from lpr mice were significantly down-modulated compared to those from +/+ mice and freshly obtained T cells. Besides, the reduction of bcl-2 protein levels was inhibited in T cells cultured in the presence of T cell receptor (TCR) signalling. These results suggest that lpr T cells might be susceptible to apoptosis in vitro due to down-modulation of bcl-2 by withdrawal of TCR signalling.

Original languageEnglish
Pages (from-to)283-288
Number of pages6
JournalApoptosis
Volume2
Issue number3
DOIs
Publication statusPublished - 1997
Externally publishedYes

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmaceutical Science
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Cancer Research

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