Related Experiment Video

Updated: Aug 9, 2026

Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS
08:38

Quantification of the Immunosuppressant Tacrolimus on Dried Blood Spots Using LC-MS/MS

Published on: November 8, 2015

Cigarette tar phenols impede T cell cycle progression by inhibiting cyclin-dependent kinases

Ashley A Frazer-Abel1, Jesica M McCue, Sabine Lazis

  • 1Division of Allergy and Clinical Immunology, University of Colorado at Denver and Health Sciences Center, Denver, CO 80262, USA.

Molecular Immunology
|April 6, 2006
PubMed

Insights

Cigarette smoke phenols, particularly hydroquinone, disrupt T cell cycle progression by inhibiting key cell cycle regulators (cyclin-dependent kinases). This finding explains how smoking impairs immune function and increases infection risk.

Area of Science:

  • Immunology
  • Molecular Biology
  • Toxicology

Background:

  • Cigarette smoking suppresses pulmonary T cell responses, increasing susceptibility to infections and reducing tumor surveillance.
  • Phenolic compounds in cigarette tar are known to inhibit T cell blastogenesis and interfere with cell cycle progression.

Purpose of the Study:

  • To elucidate the mechanism by which cigarette smoke phenolic compounds induce T cell cycle arrest.
  • To investigate the effects of these compounds on cyclin-dependent kinases (Cdks) controlling the G0/G1 transition.

Main Methods:

  • Examined the impact of hydroquinone, catechol, and phenol on Cdk4 and Cdk6 kinase activities and protein expression.
  • Assessed the effect of hydroquinone on cyclin D3 expression and Cdk6/Cyclin D3 complex formation.

Main Results:

  • Hydroquinone inhibited Cdk4 and Cdk6 kinase activities by over 80%.
  • Hydroquinone significantly reduced cyclin D3 expression (>90%), impairing Cdk6/Cyclin D3 complex formation.
  • Catechol and phenol showed markedly less potent inhibitory effects.

Conclusions:

  • Hydroquinone is a potent inhibitor of Cdk4/Cdk6 activity, crucial for T cell cycle progression.
  • Impaired Cdk6/Cyclin D3 complex formation due to hydroquinone contributes to smoking-induced T cell dysfunction.
  • Understanding these mechanisms can inform strategies to mitigate smoking-related immune suppression.

More Related Videos

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries08:49

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

Published on: January 22, 2019

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Chronopharmacokinetics: Time-Dependent Pharmacokinetics01:20

Chronopharmacokinetics: Time-Dependent Pharmacokinetics

Chronopharmacokinetics studies the temporal change in drug absorption and elimination. These changes can be cyclical or non-cyclical. Cyclical changes occur over a regular interval, while non-cyclical changes occur over a longer, irregular period.
Time-dependent pharmacokinetics refers to non-cyclical changes in drug rate processes over a period of time. It can lead to nonlinear pharmacokinetics, where the relationship between drug concentration and time is not proportional. Non-cyclical...
Drugs that Stabilize Microtubules01:15

Drugs that Stabilize Microtubules

Microtubules are dynamic structures that undergo cycles of catastrophe and rescue. The microtubules play a central role in cell division by forming the spindle apparatus for segregating the chromosomes. This makes them ideal targets for regulating dividing cells in tumors and malignant cancer cells. Microtubule stabilizing drugs help stabilize the microtubule formation and promote its polymerization. Paclitaxel was the first microtubule stabilizing agent used as anticancer drug in chemotherapy...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.