Interleukin 10 And Its Receptor

Vijay P Khatri, Division of Surgical Oncology, Roswell Park Cancer Institute, Buffalo, New York, USA

Michael A Caligiuri, Department of Hematology/Oncology, Arthur G. James Comprehensive Cancer Center, Ohio State University Medical Center, Columbus, Ohio, USA

Interleukin 10 (IL-10) is an important immunoreg-ulatory cytokine which was initially known as the cytokine synthesis inhibiting factor (CSIF) and its discovery was based upon characterization of its biological activity. Fiorentino described a type 2 T helper (TH2) cell-derived factor that could selectively inhibit the secretion of interferon 7 (IFN7) by type 1 T helper (T Hl) cells. Murine Ly-1+ B cell lymphomas were shown to have a 'B cell-derived growth factor' activity that strongly enhanced IL-2-or IL-4-dependent thymocyte proliferation. O'Garra demonstrated that the same murine lymphoma supernatant also had mast cell growth factor activity. Based on these biological activities, cDNA encoding mouse IL-10 (mIL-10) was isolated from an concava-lin A-activated TH2 clone. Subsequently, the human IL-10 (hIL-10) was identified by screening a tetanus toxin-specific human T cell cDNA library using probes based on the mouse cDNA sequence.

18.5 kDa acid-sensitive protein that belongs to the four a-helical bundle cytokine superfamily. Unlike murine IL-10, which is glycosylated at the N-ter-minus, hIL-10 lacks detectable carbohydrate moieties. This N-linked glycosylation is, however, not necessary for its biological activity. Both mIL-10 and hIL-10 protein contain intrachain disulfide bonds that are essential for the biological activity of this cytokine. hIL-10 has been shown to be active on both murine and human cells, but mIL-10 is not active on human cells. Interestingly, both the mlL-10 and hIL-10 exhibit a strong DNA (71%) and amino acid sequence (84%) homology to the open reading frame in the Epstein-Barr virus (EBV) genome called BCRF-1. Since hIL-10 and BCRF-1 (viral IL-10) are closely related in the amino acid sequence, it is postulated that EBV may have captured this mammalian gene during evolution to confer survival advantage.

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