Conti P, Youinou P, Theoharides T C
Immunology Division, Department of Oncology and Neuroscience, University of Chieti, Via dei Vestini, 66100 Chieti, Italy.
Autoimmun Rev. 2007 Jan;6(3):131-7. doi: 10.1016/j.autrev.2006.08.015. Epub 2006 Oct 16.
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 autoimmunity 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-1beta, 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.
白细胞介素（IL）和其他细胞因子具有多种重叠的能力，可刺激不同谱系和分化阶段的细胞。最值得注意的是，IL-1、肿瘤坏死因子（TNF）-α、IL-6、IL-15、IL-17、IL-18、IL-21、IL-25、IL-31和IL-32共同促成病理生理事件。这些事件包括细胞死亡、炎症、过敏和自身免疫。辅助性T（TH）1细胞或TH2细胞的上调具有致病性，并且这些亚群相互下调。内皮细胞趋化因子/细胞因子的表达对于通过将炎性T细胞运输到中枢神经系统而引发自身免疫也至关重要。IL-32（以前称为NK转录本4）是由丝裂原激活的淋巴细胞、干扰素-γ激活的上皮细胞以及IL-12、IL-18和IL-32激活的NK细胞产生的最新炎性细胞因子。它可诱导参与多种自身免疫性疾病的TNF-α、IL-1β、IL-6和2种C-X-C趋化因子家族成员。此外，IL-32通过刺激前列腺素的释放来激活外周血单核细胞中的花生四烯酸代谢。这种补充性炎性细胞因子的发现使炎症网络更加复杂。
