Recurrent allergic reactions to latex in a hospitalized pediatric patient

capable of inducing an increase in G R Kd, that is, a decrease in G R binding atfinity, in PBMCs of normal subjects similar to the alteration identified in PBMCs from patients with AD. This alteration is reversed when PBMCs from patients with A D are incubated in the absence of cytokines and sustained by the addition of IL-2 and IL-4. Therefore the observed G R binding abnormalities appear to be an acquired defect, which may be the result of ongoing immune activation and increased cytokine generation. Of note, Herscher et al. 6 have repor ted that circadian changes in endogenous glucocort icoid concentra t ions modula te the magni tude of latephase allergic responses. On the basis of these findings, we speculate that decreased G R binding atfinity in A D might blunt the antiinflamrnatory response to endogenously secreted cortisol and thus be important in perpetuating chronic immune activation and allergic inflammation. More importantly, our results may account for the variable therapeutic response to steroids found in patients with AD. REFERENCES