COMPARISON OF CHANGES IN THE PERCENTAGES OF CD8+CD28-TCRαβ+ T CELL SUBPOPULATIONS IN ALLERGIC ASTHMA SUBJECTS vs CONTROLS BEFORE AND AFTER ANTI-CD3/ANTI-CD28/IL-2 STIMULATION IN VITRO

M. Eusebio, L. Kraszula, M. Kupczyk, P. Kuna, M. Pietruczuk

Article ID: 6072
Vol 27, Issue 4, 2013
DOI: https://doi.org/10.54517/jbrha6072
Received: 8 January 2014; Accepted: 8 January 2014; Available online: 8 January 2014; Issue release: 8 January 2014

Abstract

Asthma is a chronic inflammatory disease characterized by the migration of activated T cells into the bronchial mucosa. TGF-beta and IL-10 have proved to regulate airway hyper-responsiveness and leukocytes recruitment to the airways of ovalbumin (OVA) sensitized mice. We examined relative changes in CD8+T cell subpopulations between fifty allergic asthma subjects and twenty five aged-matched healthy adults before and after anti-CD3/CD28 and IL-2 stimulation in the presence of IL-10 or TGF-beta, focusing on CD62L and FoxP3 expressing TCR alpha beta + cells. Severe asthma group had a significantly higher percentage of CD8+ CD28-and CD8+ CD28-TCR alpha beta + CD62L highFoxP3 bright T cells than other groups after enrichment. Compared to the baseline, co-stimulation with either IL-10 or TGF-beta increased the percentage of CD8+CD28-but decrease the percentage of CD8+CD28+T cells within anti-CD3/anti-CD28/IL-2 activated CD8+T cells in all groups. Co-stimulation with anti-CD3/anti-CD28/IL-2 in presence of either IL-10 or TGF-beta decreased the frequencies of CD8+CD28-TCR alpha beta +CD62Lhigh FoxP3 bright T cells in severe asthma subgroup but increased this parameter in other groups. We suggest that altered high level expression of CD62L and FoxP3 on CD8+ CD28-TCR alpha beta + T cell is relevant to allergic asthma. These data have implications for further characterization of CD8+ CD28-TCR alpha beta+ T cell subsets, with special emphasis on their implication in healthy or allergic immune response.


Keywords

IL-10;TGF-ß;FoxP3;anti-CD3/CD28;CD8+TCRαβ+ T cells;allergic asthma


References

Supporting Agencies



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