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Related Experiment Videos

TCR and immunophenotype changes in dimethyl sulfoxide-dependent programmed cell death.

O Trubiani1, P De Fazio, M Ciancarelli

  • 1Department of Odontostomatology, University of Chieti, Italy.

Journal of Biological Regulators and Homeostatic Agents
|February 24, 2001
PubMed
Summary

Dimethyl sulfoxide (DMSO) enforces T-cell receptor (TCR) expression in pre-T cells, triggering apoptosis and altering immunophenotypes. This suggests an early checkpoint in T-cell differentiation and programmed cell death.

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Area of Science:

  • Immunology
  • Cell Biology
  • Developmental Biology

Background:

  • The thymus is crucial for T-cell receptor (TCR) repertoire development, involving significant cell death of immature thymocytes.
  • Somatic gene rearrangements create functional TCR recognition units, essential for T-cell activation, growth, and differentiation.
  • Previous studies showed dimethyl sulfoxide (DMSO) induces apoptosis in RPMI-8402 human pre-T cells.

Purpose of the Study:

  • To investigate the effects of DMSO on pre-T cells undergoing negative selection.
  • To analyze DMSO-induced changes in T-cell receptor expression and immunophenotype.
  • To explore the link between TCR regulation, immunophenotypes, and programmed cell death in T-cell differentiation.

Main Methods:

  • Treatment of pre-T cells with DMSO.

Related Experiment Videos

  • Analysis of cell growth inhibition and immunophenotype modulation (CD2, CD7 expression).
  • Assessment of TCR chain expression (alpha/beta, gamma/delta) and related enzyme activity (TdT, RAG-1, RAG-2).
  • Evaluation of apoptotic program induction.
  • Main Results:

    • DMSO induced significant cell growth inhibition in pre-T cells.
    • DMSO caused immunophenotype changes, including down-regulation of CD2 and CD7.
    • DMSO increased alpha/beta or gamma/delta TCR chain expression, associated with TdT, RAG-1, and RAG-2 activity.
    • These DMSO-induced modifications were linked to an apoptotic program.

    Conclusions:

    • DMSO enforces TCR expression in pre-T cells, leading to cell growth inhibition and apoptosis.
    • DMSO treatment modulates immunophenotypes and TCR chain expression, indicating its role in T-cell differentiation.
    • These findings suggest an early intrathymic checkpoint regulating T-cell differentiation, linking immunophenotypes, TCR regulation, and programmed cell death.