Mini reviewA gradient of glucocorticoid sensitivity among helper T cell cytokines

- Th1 cells are sensitive to glucocorticoid-induced apoptosis and cytokine suppression.
- Th2 cells are sensitive to glucocorticoid suppression of cytokines but resistant to glucocorticoid-induced apoptosis.
- Th17 cells are resistant to glucocorticoid-induced apoptosis and cytokine suppression.
- Underlying Th cells mediate distinct glucocorticoid responsiveness and severity of diseases.
- Th cells have cell and promoter-specific glucocorticoid receptor signaling.

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.