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).