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Updated: Feb 5, 2026

Measuring Mitochondrial Function of Naïve and Effector CD8 T Cells
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CD28

Alejandra Pera1,2, Stefano Caserta3, Fabio Albanese1

  • 1Department of Clinical and Experimental Medicine, Brighton and Sussex Medical School, Brighton, United Kingdom.

Theranostics
|September 15, 2018
PubMed
Summary

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This summary is machine-generated.

Cytomegalovirus (CMV) infection, not aging, drives the expansion of CD28null T-cells, increasing cardiovascular risk. This finding highlights CMV infection as a key factor in T-cell associated cardiovascular pathology.

Area of Science:

  • Immunology
  • Cardiovascular Science
  • Virology

Background:

  • Cytomegalovirus (CMV) infection is linked to increased cardiovascular mortality, potentially via CD28null T-cell accumulation.
  • CD28null T-cells, particularly CD28null CD4 T-cells, can damage endothelium and precipitate cardiovascular events.
  • The accumulation of CD28null T-cells is traditionally attributed to aging, with CMV's role explained by its higher prevalence in older individuals.

Purpose of the Study:

  • To determine whether Cytomegalovirus (CMV) infection or aging is the primary driver of CD28null T-cell accumulation.
  • To investigate the association between CMV infection, aging, HLA type, and the expansion of CD28null CD4 and CD8 T-cells.
  • To clarify the mechanisms underlying the increased cardiovascular risk in CMV-infected individuals.

Main Methods:

Keywords:
CD28null CD4 T-cellsCD28null CD8 T-cellsCytomegalovirusagingcardiovascular diseasecoronary complications

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  • Multi-color flow cytometry was employed to quantify CD28null T-cell subsets (CD4 and CD8).
  • Antigen-specific activation assays and HLA-typing were utilized to analyze T-cell responses and genetic factors.
  • Linear and logistic regression models assessed the influence of sex, age, CMV infection status, and HLA type on T-cell frequencies.

Main Results:

  • CMV-positive individuals exhibited significantly higher frequencies of CD28null CD4 T-cells (>12-fold) and CD28null CD8 T-cells (~2-fold) compared to CMV-negative individuals.
  • Aging had a minimal impact on CD28null T-cell expansion, primarily observed in CMV-positive individuals.
  • The presence of HLA-DRB1*0301 was associated with a substantial reduction in the risk of CD28null CD4 T-cell expansion (OR=0.108).

Conclusions:

  • Cytomegalovirus (CMV) infection is a major determinant of CD28null CD4 T-cell accumulation and associated cardiovascular pathology.
  • Increased CD28null CD8 T-cell counts are also linked to CMV infection, though to a lesser extent.
  • HLA type, specifically HLA-DRB1*0301, plays a protective role against CD28null CD4 T-cell expansion, suggesting new avenues for risk assessment and treatment.