Glucocorticoid-resistant asthma. T-lymphocyte defects.

There is adequate evidence that clinical glucocorticoid resistance in asthma can be attributed at least partly to a relative resistance of T cells to inhibition by glucocorticoids. Although GR asthma defined according to the present criteria represents one end of a spectrum of clinical response, in clinical practice these patients would not be exposed for prolonged periods to dosages of glucocorticoids sufficient to inhibit their T cells in vivo. A more rational approach to the selection of alternative therapy for such patients might be possible when the mechanisms of this resistance are identified. In the meantime, there is some justification for assessing other drugs that inhibit T cells from patients with GR asthma at therapeutic concentrations for their efficacy and risk/benefit ratios in clinical practice.