The anti-inflammatory mechanism of Astragaloside in the recurrences of asthma mice

The recurrence of asthma is partly mediated by allergen-specific CD4 memory T cells that promote lung inflammation through recruitment of cellular effectors into the lung. Central memory T cells(Tcm), a subset of memory T cells following infection and allergen induction, can rapidly response to the allergen and produce inflammatory production which is the important role of the recall of allergy response. Targeting the expansion of pathogenic central memory immune cells is a promising therapeutic strategy to prevent chronic autoimmune recurrence. However, current common therapies cannot alter the frequency of central memory T cells subsets in adult atopic asthma patients. We previously carried out an animal study, which showed that Astragaloside (AST) could inhibit the recurrences of asthma attack, however, the underlying therapeutic mechanism were not completely clear. The important question of this research is whether AST, as an anti-inflammatory agent used in asthma therapy, may act on the memory T-cell subpopulation to prevent the recurrences of asthma attack. In this study, we dissect the treatment effectiveness and mechanism of AST on Tcms from generation and migration in the recurrences of asthma.