Effects of cigarette smoke extract on primary activated T cells

Cell Immunol. 2013 Mar;282(1):38-43. doi: 10.1016/j.cellimm.2013.04.005. Epub 2013 Apr 22.


Tobacco smoking predisposes the development of diseases characterized by chronic inflammation and T cell dysfunction. In this study, we aimed to determine the direct effects of cigarette smoke on primary T cells and to identify the corresponding molecular mediators. Activated T cells cultured in the presence of cigarette smoke extract (CSE) displayed a dose-dependent decrease in cell proliferation, which associated with the induction of cellular apoptosis. T cell apoptosis by CSE was independent of caspases and mediated through reactive oxygen and nitrogen species endogenously contained within CSE. Additional results showed that exposure of T cells to CSE induced phosphorylation of the stress mediator eukaryotic-translation-initiation-factor 2 alpha (eIF2α). Inhibition of the phosphorylation of eIF2α in T cells prevented the cellular apoptosis induced by CSE. Altogether, the results show the direct effects of CSE on T cells, which advance in the understanding of how cigarette smoking promotes chronic inflammation and immune dysfunction.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Blotting, Western
  • Cell Proliferation / drug effects*
  • Cells, Cultured
  • Culture Media, Serum-Free / chemistry
  • Culture Media, Serum-Free / pharmacology*
  • Dose-Response Relationship, Drug
  • Eukaryotic Initiation Factor-2 / metabolism
  • Flow Cytometry
  • Humans
  • Lymphocyte Activation / immunology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Phosphorylation / drug effects
  • Reactive Oxygen Species / chemistry
  • Reactive Oxygen Species / metabolism
  • Smoke*
  • T-Lymphocytes / cytology
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / immunology
  • Tobacco / chemistry*


  • Culture Media, Serum-Free
  • Eukaryotic Initiation Factor-2
  • Reactive Oxygen Species
  • Smoke