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This article is part of the supplement: Interleukin-6, a pleiotropic cytokine

Highly Accessed Review

Interleukin-6: discovery of a pleiotropic cytokine

Tadamitsu Kishimoto

Author Affiliations

Laboratory of Immunoregulation, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan

Arthritis Research & Therapy 2006, 8(Suppl 2):S2  doi:10.1186/ar1916

Published: 28 July 2006

Abstract

In the late 1960s, the essential role played by T cells in antibody production was reported. This led to our hypothesis that certain molecules would have to be released from T cells to effect the stimulation of B cells. This hypothesis was shown to be true. There were certain factors present in the culture supernatant of T cells that induced proliferation and differentiation of B cells. The factor that induced B cells to produce immunoglobulins was initially named B cell stimulatory factor-2. The cDNA encoding the human B cell stimulatory factor-2 was cloned in 1986. At the same time, IFN-β2 and a 26 kDa protein in the fibroblasts were independently cloned and found to be identical to B cell stimulatory factor-2. Later, a hybridoma/plasmacytoma growth factor and a hepatocyte stimulating factor were also proven to be the same molecule as B cell stimulatory factor-2. Various names were used for this single molecule because of its multiple biological activities, but these have all been unified and the molecule is now known as IL-6. Since the discovery of IL-6, rapid progress has been made in our understanding of IL-6 activities, the IL-6 receptor system and the IL-6 signal transduction mechanism. More importantly, it has been shown to be involved in a number of diseases such as rheumatoid arthritis and Castleman's disease. When taking into account all the accumulated basic research on the various aspects of this molecule, it appeared that blocking the activity of IL-6 was a feasible, new therapeutic approach for chronic inflammatory diseases.