Answer: b IL-1 and TNFa share many biologic properties. In addition, each potentiates the effects of the other one when given concurrently. Overall, IL-1 alone probably has weaker effects than TNFa with respect to the induction of shock; its role is likely to be important with respect to its marked potentiating abilities as it relates to TNFa. IL-1 expression is regulated by a host of factors including IL-2, granulocyte macrophage colony stimulating factor (GM-CSF), transforming growth factor b (TGF-b), TNFa, all of the interferons, and IL-1 itself. Other endogenous stimuli for IL-1 production include antigen-antibody complex, the Fc region of IgG, and C5a; other nonspecific exogenous stimuli include silica particles and UV irradiation. One of the key proinflammatory features of IL-1-induced inflammation is the stimulation of arachadonic acid metabolism. IL-1 stimulates the release of pituitary stress hormones and increases the synthesis of collagenases, resulting in the destruction of cartilage, bone and other collagen-rich structures. IL-1 stimulates prostaglandin production. One of the most important properties of IL-1 involves its interaction with the vascular endothelium. This includes the adherence of neutrophils, basophils, eosinophils, monocytes, and lymphocytes to the vascular endothelium via interaction between adhesion molecules on leukocytes and adhesion-receptor complex on the endothelial cells. By inducing the expression of ICAM-1, E-selectin, and VCAM-1 on endothelial cells, IL-1 provides a key step in the extravasation of leukocytes to sites of local inflammation and injury