Modulation of autoimmunity by the latest interleukins (with special emphasis on IL-32)

Interleukins (IL) and other cytokines display a number of overlapping abilities to stimulate cells of various lineages and differentiation stages. Most notably, IL-1, tumor necrosis factor (TNF)-alpha, IL-6, IL-15, IL-17, IL-18, IL-21, IL-25, IL-25, IL-31 and IL-32 contribute in concert to pathophysiological events. These include cell death, inflammation, allergy and autoimmunity. Up-regulation of either T helper (TH)1 or TH2 cells is pathogenic, and these subsets downregulate each other. The expression of chemokines/cytokines by endothelial cells is also crucial to autoinummity by trafficking inflammatory T cells into the central-nervous system. IL-32 (previously termed NK transcript 4), is the newest inflammatory cytokine produced by mitogen-activated lymphocytes, interferon-gamma activated epithelial cells and IL-12, IL-18 and IL-32-activated NK cells. This induces TNF-alpha, IL-1 beta, IL-6 and 2 C-X-C chemokine family members involved in several autoimmune (.) diseases. In addition, IL-32 activates arachidonic acid metabolism in peripheral blood mononuclear cells by stimulating the release of prostaglandins. Discovery of this supplementary inflammatory cytokine further complicates the network of inflammation. (c) 2006 Elsevier B.V. All rights reserved.