Abstract
Interleukin-2 (IL-2) was first described as a T-cell growth factor (TCGF) in 1976 by Morgan et al. when it was noted that conditioned medium could support T-cell growth (1). IL-2 was later demonstrated to have no direct antitumor activity, but to mediate antitumor activity indirectly through the host immune response (2, 3). The primary source of IL-2 is from an antigen-stimulated TH1-type CD4+ T cell and, to a lesser extent, from activated CD8+ cells (4). At least two external signals are required for T-cell activation, one through the T-cell receptor complex (TCR/CD3+), and the second from an accessory cell expressing B7, a ligand for the T-cell CD28+ receptor. It is encoded on chromosome 4q26–28 (5) and was first cloned in 1983 (6). IL-2 is a 15 kD protein consisting of two paired α helices bound by an interchain di-sulfide bond between cysteine residues at positions 58 and 105. IL-2 interacts with the T-cell IL-2 Rβγ heterodimer at the receptor, the structure of which is similar to that of IL-4 and GM-CSF (7).
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Olencki, T., Bukowski, R.M. (2000). Interleukin-2 in Metastatic Renal Cell Carcinoma. In: Bukowski, R.M., Novick, A.C. (eds) Renal Cell Carcinoma. Current Clinical Oncology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-229-6_19
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