免疫学
白细胞介素23
免疫系统
自身免疫
实验性自身免疫性脑脊髓炎
炎症
生物
背景(考古学)
细胞因子
白细胞介素17
促炎细胞因子
肿瘤坏死因子α
先天性淋巴细胞
医学
获得性免疫系统
白细胞介素15
先天免疫系统
白细胞介素10
古生物学
作者
Brent McKenzie,Robert A. Kastelein,J. Daniel
标识
DOI:10.1016/j.it.2005.10.003
摘要
Interleukin (IL)-23 is a heterodimeric cytokine closely related to IL-12. Yet, despite a strong structural relationship that includes a shared p40 subunit, this does not translate into functional similarity. In fact, the opposite is true, in that these two cytokines appear to have profoundly different roles in regulating host immune responses. It is now clear that IL-23 has key roles in autoimmune destruction in experimental allergic encephalomyelitis, collagen-induced arthritis and inflammatory bowel disease. IL-23 drives the development of autoreactive IL-17-producing T cells and promotes chronic inflammation dominated by IL-17, IL-6, IL-8 and tumor necrosis factor as well as neutrophils and monocytes. It is unlikely that IL-23 and its downstream effects evolved just to cause autoimmunity, but its real benefit to the host and the lineage relationship between IL-17-producing cells and T helper 1 cells remain unclear. By comparing the pathophysiological function of IL-12 and IL-23 in the context of host defense and autoimmune inflammation, we are beginning to understand the novel IL-23-IL-17 immune pathway.
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