IL-18, is known as the IFN gamma-inducing factor, and as a proinflammatory cytokine, a member of the IL-1 family. Initially it is produced as an inactive pro-form and then secreted following maturation by caspase-1. IL-18 binds to the IL-18 receptor α (IL-18Rα) expressed on the surface of various cells (Kupffer cells, activated macrophages, keratinocytes, intestinal epithelial cells, osteoblasts, adrenal cortex cells and murine diencephalon) leading to inflammation. IL-18 also acts on T helper type-1 (Th1) T cells and in combination with IL-12 strongly induces them to produce IFN-γ. IL-18 has pleiotropic effects from enhancement production of IFN-γ and GM-CSF in peripheral blood mononuclear cells to production of Th1 cytokines, IL-2, GM-CSF and IFN-γ in T cells as well as the enhancement of Fas ligand expression by Th1 cells. Consequently, researchers are exploiting these regulatory processes for anti-tumor immune responses as IL-18 enhances antitumor immunity in various cancer types. The powerful activity of IL-18 in tumor models has emphasized the great attraction of IL-18 pathway as a target for tumor immunotherapy.

IL-18 MBL

Researchers take advantage of MBL International recombinant IL-18 to activate varying cells like peripheral blood cells, macrophages, NK cells and T cells to identify targets.

For ex vivo studies, MBLI provides formulation without BSA. In addition, we offer other IL-18 products, in turn, we have become a trusted leader in IL-18 research worldwide.

Product Highlights:

Article number Product description Size
B004-2 Recombinant Mouse IL-18 (Without BSA) 200 μg
B004-5 Recombinant Mouse IL-18 (Without BSA) 25 μg
B003-5 Recombinant Human IL-18 (without BSA) 25 μg
B003-2 Recombinant IL-18 (without BSA) 200 μg

References

  1. Ohya, Takashi, et al. “Impaired Interleukin‐18 Signaling in Natural Killer Cells from Patients with Systemic Juvenile Idiopathic Arthritis.” ACR Open Rheumatology, vol. 4, no. 6, 2022, pp. 503–510., doi:10.1002/acr2.11426.
  2. Wang, Zhen, et al. “Interleukin-37 Promotes Colitis-Associated Carcinogenesis via SIGIRR-Mediated Cytotoxic T Cells Dysfunction.” Signal Transduction and Targeted Therapy, vol. 7, no. 1, 2022, doi:10.1038/s41392-021-00820-z.
  3. Tsutsuki, Hiroyasu, et al. “Subtilase Cytotoxin from Shiga-Toxigenic Escherichia Coli Impairs the Inflammasome and Exacerbates Enteropathogenic Bacterial Infection.” IScience, vol. 25, no. 4, 2022, p. 104050., doi:10.1016/j.isci.2022.104050.
  4. Stone, Deborah L., et al. “Excess Serum Interleukin‐18 Distinguishes Patients with Pathogenic Mutations in pstpip1 .” Arthritis & Rheumatology, vol. 74, no. 2, 2022, pp. 353–357., doi:10.1002/art.41976.

For Research Use Only. Not for use in diagnostic procedures.