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IL-32, a novel cytokine with a possible role in disease
  1. C A Dinarello1,
  2. S-H Kim2
  1. 1University of Colorado Health Sciences Center, Denver, CO, USA
  2. 2Department of Biomedical Science and Technology, Konkuk University, Seoul, Korea
  1. Correspondence to:
    Dr C Dinarello
    University of Colorado, Health Science Center, 4200 East Ninth Avenue, 80262 Denver, CO, USA; cdinare333{at}


IL-32 is the name given to the NK4 transcript first reported in IL-2 activated T lymphocytes and natural killer cells 13 years ago without known function. The novel cytokine has six isoforms. In an study to isolate a soluble form of the IL-32 receptor from human urine, IL-32α bound proteinase-3 with high affinity and was not affected by enzyme inhibition. IL-32α/IL-32γ were expressed as recombinant molecules. The cytokine exhibits properties characteristic of proinflammatory cytokines and also induces the degradation of inhibitory κB and phosphorylation of mitogen activated protein p38. Monoclonal antibodies to IL-32 identify its presence in a variety of human tissues from diseases states. Epithelial cells from healthy subjects express low levels of the cytokine, but in disease conditions such as chronic obstructive pulmonary disease, Crohn’s disease and psoriasis, the expression increases markedly. IL-32 is a major transcript in gene array studies in epithelial cells stimulated with IFNγ in vitro. In rheumatoid arthritis, synovial tissues reveals increased content of IL-32, which correlates with severity of disease. A highly significant correlation has been observed between the number of synovial and macrophagic cells positive for IL-32 and the level of erythrocytes sedimentation, IL-1β, tumour necrosis factor α, and IL-18. Thus, IL-32 exhibits many properties of proinflammatory cytokines and associations with disease severity.

  • FLS, fibroblast-like synoviocytes
  • IL, interleukin
  • MCP, monocyte chemoattractant protein
  • NOD, nuclear oligomerisation domain
  • NK, natural killer
  • PAR, proteinase activated receptor
  • PMSF, phenylmethylsulphonyl fluoride
  • PR3, proteinase 3
  • RA, rheumatoid arthritis
  • TNF, tumour necrosis factor
  • TLR, toll-like receptor
  • interleukin
  • IL-32
  • cytokine
  • rheumatoid arthritis

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  • These studies are supported by NIH Grants AI-15614 (CAD), HL-68743 (CAD), and CA-04 6934 (CAD), and Amgen, Inc.

  • Competing interests: none declared

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