Interleukin 1 (IL-1) is considered the first of the super-family of regulatory and inflammatory cytokines. There are two distinct IL-1 proteins: Interleukin 1α and Interleukin 1b. The two forms of IL-1 are distinct gene products; they recognize the same receptor and share biological properties. IL-1 has a number of alternative names, including lymphocyte activating factor, endogenous pyrogen, catabolin, hemopoietin-1, melanoma growth inhibition factor, and osteoclast activating factor. The properties and biological activities of IL-1 have been extensively reviewed. IL-1 is expressed by many cells and has multiple functions including local inflammation. Cells known to express IL-1b include astrocytes, adrenal cortical cells, natural killer (NK) cells, macrophages and monocytes, endothelial cells, keratinocytes, megakaryocytes and platelets, neurons, neutrophils,oligodendroglia, osteoblasts, Schwann cells, trophoblasts, and T cells plus fibroblasts. The biological properties of IL-1 show some overlap with other cytokines including tumor necrosis factor (TNF) and interleukin 6 (IL-6), which are all capable of stimulating T and B lymphocytes, augmenting cell proliferation and initiating or suppressing gene expression for several proteins. Although IL-1 is generally thought of as a prototypical pro-inflammatory cytokine, the effects of IL-1 are not limited to inflammation. Following bacterial or immunoglobulin ligation of monocyte/macrophage CD14 (the LPS receptor) or CD64 (the IgG receptor), IL-1 can be released into a local environment. Within this environment, IL-1 impacts a number of cells. First, capillary endothelial cells are induced to do two things, one, secrete chemokines such as MCP-1, and two, up-regulate the expression of vascular adhesion molecules such as E-Selectin, ICAM-1 and VCAM-1. MCP-1 provides a stimulus for chemotaxis and activates mononuclear cell integrins, thus facilitating mononuclear infiltration into an area of early inflammation. IL-1 also induces expression of itself in newly arriving monocytes, thus reinforcing the overall process. In terms of other pro-inflammatory molecules, IL-1 apparently is needed for the efficient production of IFN-g. On resident NK cells, IL-1 apparently works in conjunction with macrophage-derived IL-12 to induce IFN-g secretion, resulting in an IFN-g induced activation of macrophages. Finally, IL-1 also induces the expression of MMPs from resident fibroblasts. This function can have at least two effects: first extracellular matrix degradation can facilitate monocyte migration, and second, MMPs are known to degrade IL-1b, thus down-modulating the local inflammatory response initiated by IL-1. This IL-1b ELISA is a ready-to-use 3.5-hour solid phase immunoassay capable of measuring IL-1b levels in cell culture supernatant, serum, plasma, and other biological fluids in the range of 0 to 400 pg/mL. This assay has shown no cross-reactivity with various other cytokines super-family proteins.