The effects of glucocorticoids on human eosinophils

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Presentation transcript:

The effects of glucocorticoids on human eosinophils Robert P. Schleimer, PhD, Bruce S. Bochner, MD Journal of Allergy and Clinical Immunology Volume 94, Issue 6, Pages 1202-1213 (December 1994) DOI: 10.1016/0091-6749(94)90333-6 Copyright © 1994 Mosby, Inc. Terms and Conditions

FIG. 1 Influence of the potent glucocorticoid dexamethasone on survival of human peripheral blood eosinophils in vitro (adapted from Lamas et al.61). Purified peripheral blood eosinophils were cultured in the presence of the indicated concentrations of GM-CSF for 6 days, after which viable cell recovery was determined. In cultures lacking cytokine, viable cell recovery was 0. Data shown are for eosinophils cultured in the simultaneous presence of GM-CSF and either dexamethasone (10–7 mol/L, filled circles) or control (an equivalent amount of dimethyl sulfoxide vehicle, filled squares). Journal of Allergy and Clinical Immunology 1994 94, 1202-1213DOI: (10.1016/0091-6749(94)90333-6) Copyright © 1994 Mosby, Inc. Terms and Conditions

FIG. 2 A model showing possible sites of glucocorticoid action on eosinophil survival. The model shows a supporting cell (left) and eosinophil (right), both of which are capable of producing growth factors that can maintain eosinophil survival. Possible sites of glucocorticoid action are indicated by boxes with numbers and are: (1) inhibition of the production of eosinophil survival-promoting cytokines including GM-CSF, IL-3, and IL-5 by the supporting cell and direct inhibition of autocrine production of survival-promoting factors by the eosinophil itself; and (2) prevention of the action of transcription factors, the activity of which is induced by the engagement of the hematopoietic cytokine receptor, thus preventing transcription factor–dependent processes, which induce survival, and proliferation in less mature cells. In addition, eosinophils may have an active process by which the trigger for the final common pathway of programmed cell death is suppressed. Glucocorticoids may prevent this active suppression of triggering of the final common pathway and thus facilitate entry into apoptosis. Journal of Allergy and Clinical Immunology 1994 94, 1202-1213DOI: (10.1016/0091-6749(94)90333-6) Copyright © 1994 Mosby, Inc. Terms and Conditions