Dynamics and proliferative capacities of CD8+CD28+TCRαβ+CD62Lhigh T-cell subsets in healthy and asthmatic subjects

Adhesion molecules, as such, play essential roles in T-cell transendothelial extravasation during inflammation. A better understanding of the mechanisms underlying this process may be of value in the management of asthma. The present study employed Magnetic-Activated Cell Sorting (MACS) to isolate human CD8(+) T lymphocytes from peripheral blood of asthma patients and controls. The cells were flow cytometrically assessed to evaluate surface expression of an adhesion molecule, L-selectin (CD62L) on the surface of CD8(FoxP3-/bright T) cell subsets and its response to inflammatory cytokines. We showed that CD8(+)CD28(+)TCR alpha beta(+)CD62L(high)FoxP3(bright) T cells were deficient in blood of some asthma patients but abundant in others. After co-stimulation of CD8(+) T cells with anti-CD3/CD28 in combination with IL-2 and IL-10 or TGF-beta, the frequencies of CD8(+)CD28(+)TCR alpha/beta(+)CD62L(high) T cells in the group of patients were lower than at baseline. Our data indicate that L-selectin expression is regulated by inflammatory cytokines. Overall, these data reveal that asthma phenotypes may be further stratified into micro subtypes with distinct cellular and molecular characteristics, supporting the concept of asthma endotypes.