What are the effects of Glucocorticoids on the innate and adaptive immune systems?
- • Innate immune system.
- GCs upregulate enzymes that degrade bradykinin resulting in vasoconstriction. This causes less swelling and pain.
- GCs suppress production of prostaglandins by inducing synthesis of lipocortin-1, which inhibits phospholipase A2-mediated liberation of arachidonic acid from cell membranes.
- GCs inhibit NF-κB which suppresses COX-2 synthesis. Does not affect COX-1 so platelet function is preserved.
- GCs interfere with phagocytosis and cytokine production by macrophages and neutrophils.
- Neutrophilia occurs as a result of increased release from bone marrow and decreased migration out of vasculature resulting from inhibition of adhesion molecule production and decreased cellular adherence to vessel walls.
- GCs decrease the release of eosinophils from bone marrow and increase apoptosis (eosinopenia).
- • Adaptive (acquired) immune response.
- Dendritic cells undergo increased apoptosis.
- T cells are redistributed to tissues (lymphopenia).
- Inhibits T helper, type 1 (Th1) > Th2 and Th17 cytokine production (causes anergy to tuberculosis and other skin testing).
- B cells less affected by GCs than T cells.
- Immunoglobulin production preserved unless prolonged (>1 year) of GCs at nonphysiologic doses (>12.5 mg/day prednisone).
- Monocytes redistributed to tissues (monocytopenia).
- Inhibits mast cell degranulation (affects allergy skin testing).
