Interleukin-16 (IL-16) discovered in 19821, known formerly as lymphocyte chemoattractant factor (LCF) is a lymphocyte chemoattractant factor of T cell origin with selective activity for CD4+ T cells. LCF was designated interleukin-16 (IL-16) in 1995. IL-16 is a product of CD8+ cells, CD4+ cells2, eosinophils3, mast cells and epithelial cells derived from asthmatics4. Expression of IL-16 in asthmatic epithelium correlates with the number of infiltrating CD4+ T cells5. LCF was originally identified and purified from the supernatants of ConA-stimulated peripheral blood mononuclear cells (PBMC). In addition to its chemotactic activity, it is a competence growth factor selective for CD4+ T cells dependent on an interaction with CD4 for induction of functional activity. Its cDNA codes for a novel 14-kDa protein into a homotetrameric form is required for induction of biologic activity. IL-16 appears in culture supernatants as a relative molecular mass (Mr) ~56,000 biologically active, non-covalently linked tetramer, but migrates in monomeric form in SDS PAGE. Eluted monomeric peptides are inactive but reaggregate to Mr 56,000 regaining biological activity6. The protein expressed from the IL-16 cDNA demonstrates all the functions and chemical features of the native protein, including an identical pI, and autoaggregation into functional tetramers. IL-16 is performed and stored in biologically active form in CD8+. T cells from which it is secreted following stimulation with histamine via H2 type receptors. The secretory process occurs within 4 hrs and does not require transcription, translation, or new protein synthesis. IL-16’s ability to inhibit the MLR and other antigen induced activation suggests that it may be useful in inhibiting allograft rejection. Because IL-16 selectively induces IL-2 responsiveness in CD4+ T cells it may be useful (along with IL-2) for selective CD4+ T cell immune reconstitution in individuals with lymphopenia, for example following chemotherapy or HIV-1 infection. In the latter circumstance, its ability to inhibit HIV transcription should provide a protective role if used as a therapy in HIV-1 infected individuals7. Inhibitors of IL-16 chemotactic function may be useful in diseases in which it appears to play a prominent role in the inflammatory process. The presence of IL-16 early after antigen challenge in asthma8, the marked upregulation of IL-16 synthesis by epithelium of asthmatics along with the correlation of IL-16 protein with the number of infiltrating CD4+ T cells in the airways of human asthmatics suggest that therapeutics aims at blocking IL-16 synthesis or function may be valuable in this disease. This IL-16 ELISA is a 4.5 hour solid phase immunoassay readily applicable to measure IL-16 in serum, plasma, cell culture supernatant, and other biological fluids in the range of 0 to 3200 pg/mL. It showed no cross-reactivity with other cytokines tested such as EGF, EPO, GM-CSF, IL-1β, IL-7, IL-8, IFN-γ, MCAF, MCP-3, M-CSF, SAA, TGF-β, and TNF-α.