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Dimethyl sulfoxide induces programmed cell death and reversible G1 arrest in the cell cycle of human lymphoid pre-T

O Trubiani1, M Ciancarelli, M Rapino

  • 1Istituto di Morfologia Umana Normale, Facoltà di Medicina, Università di Chieti, Italy.

Immunology Letters
|April 1, 1996
PubMed

Insights

Dimethyl sulfoxide (DMSO) selectively impacts pre-T cells, causing cell cycle arrest and apoptosis, while leaving pre-B cells unaffected. This reveals a new model for studying DMSO

Area of Science:

  • Immunology
  • Cell Biology
  • Pharmacology

Background:

  • Programmed cell death (apoptosis) is crucial for immune system regulation, including T-cell elimination and B-cell selection.
  • Dimethyl sulfoxide (DMSO) is known to affect cell proliferation and prevent apoptosis in some cell types.

Purpose of the Study:

  • To investigate the differential effects of DMSO on human pre-B and pre-T lymphoid cell lines.
  • To understand DMSO's role in regulating cell cycle progression and apoptosis in immune cells.

Main Methods:

  • Utilized undifferentiated human pre-B (KM-3) and pre-T (RPMI-8402) lymphoid cell lines.
  • Performed multiparametric analyses to assess cell cycle, differentiation, apoptosis, and terminal transferase (TdT) expression.
  • Evaluated the reversibility of DMSO-induced effects.

Main Results:

  • DMSO induced a reversible G1 cell cycle arrest specifically in the pre-T cell line.
  • A significant increase in apoptotic cells was observed in the DMSO-treated pre-T cells.
  • Terminal transferase (TdT) expression was modified in the pre-T cells following DMSO treatment.
  • The pre-B cell line demonstrated resistance to DMSO's effects on proliferation and apoptosis.

Conclusions:

  • DMSO exhibits selective effects on distinct immune cell precursors, impacting pre-T cells but not pre-B cells.
  • These findings establish a novel model for studying cell-type-specific responses to DMSO within the immune system.
  • The differential response highlights DMSO's potential as a tool to modulate specific immune cell populations.

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