Helper T (Th) cells secret specific cytokines that promote immune responses whereas glucocorticoids
limit the extent of immune responses by inhibiting cytokine secretion and other functions of Th cells.
However, glucocorticoid resistance develops in subgroups of patients with Th cell-driven diseases such as
asthma and Crohn’s disease. Recent evidence supports that Th1, Th2, and Th17 cells have distinct
glucocorticoid sensitivity. Th1 cells are sensitive to glucocorticoid-induced apoptosis and cytokine
suppression while Th2 cells are sensitive to the latter but not the former and Th17 cells are resistant to
both. This gradient of glucocorticoid sensitivity of Th cells corresponds to the glucocorticoid sensitivity of
the diseases they underlie. We identify the mechanisms contributing to distinct glucocorticoid sensitivity
of Th cells and their cytokines in the literature, as this information is useful to improve treatment
strategies for glucocorticoid resistant immunological disorders