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Published on: January 5, 2016
Expression of CD69 on T-cell subsets in HIV-1 disease
C Pitsios1, A Dimitrakopoulou, K Tsalimalma
1Department of Immunology, Laiko General Hospital, Athens, Greece. pitsios@yahoo.com
Insights
CD69 expression on T cells is reduced in individuals with AIDS and those not responding to HAART, indicating a specific impact of advanced HIV disease on T cell activation markers. Cytokine production remained unaffected in these groups.
Area of Science:
- Immunology
- Virology
- Cellular Biology
Background:
- CD69 is a key early activation marker for T lymphocytes.
- Assessing T cell activation is crucial for understanding immune status in HIV-1 infection.
- CD69 and CD28 co-expression provides insights into T cell function.
Purpose of the Study:
- To evaluate CD69 expression on CD4 and CD8 T lymphocytes in HIV-1 infected individuals.
- To investigate the co-expression of CD69 and CD28 on T cells.
- To analyze cytokine production in CD69-expressing T cells in response to stimulation.
Main Methods:
- Whole-blood flow cytometry was employed to measure CD69 and CD28 expression.
- T cells were stimulated with phytohemagglutinin (PHA) or anti-CD3/CD28 antibodies.
- Cytokine production (IL-2, IFN-gamma) was assessed in stimulated T cells.
Main Results:
- Lower CD69 expression on CD4 T cells was observed in AIDS and HAART non-responders compared to controls.
- A decrease in CD69(+)CD28(+) T cells was noted in AIDS patients post-stimulation.
- No significant differences in IL-2 or IFN-gamma production were found between HIV-1 positive and healthy individuals.
Conclusions:
- CD69 expression is significantly affected in the advanced stages of HIV-1 infection (AIDS) and in patients non-responsive to HAART.
- The observed reduction in CD69 and CD69/CD28 co-expression suggests impaired T cell activation in severe HIV-1 disease.
- Cytokine production capacity of T cells appears preserved even with altered CD69 expression patterns in HIV-1 infection.
Abstract:
CD69 is the earliest activation marker newly synthesized and expressed during T lymphocyte activation. In this study, a whole-blood flow-cytometry-based assay was used to assess expression of the activation antigen CD69 on CD4 and CD8 T lymphocytes, and the co-expression of CD69 and CD28 on T cells. The expression of CD69 was studied in both unstimulated and in phytohaemagglutinin (PHA)- or anti-CD(3)/CD(28)-stimulated, 4-h culture, samples. The production of IL-2, IFN-gamma or both cytokines, in CD69(+) T cells, in response to Staphylococcus enterotoxin B was also tested. Fifty-three HIV-1-infected and 21 healthy volunteers participated in this study. In both PHA- and anti-CD(3)/CD(28)-stimulated cultures the percentage of CD69 on CD3(+)CD4(+) T cells was significantly lower in AIDS (and non-responders to HAART) versus healthy controls and the other HIV-1(+) groups. A decrease of CD69(+)CD28(+) T cells after PHA or MoAbs stimulation is noticed in AIDS. No difference in cytokine production was noticed between healthy volunteers and HIV-1(+) patients. Our results suggest that the expression of CD69 is affected only in the AIDS stage and in the non-responders to HAART patients.
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