Trinchieri G
The Wistar Institute of Anatomy and Biology, 3601 Spruce Street, Philadelphia, PA 19104, USA.
Curr Opin Immunol. 1997 Feb;9(1):17-23. doi: 10.1016/s0952-7915(97)80154-9.
The three cytokines IL-12, IL-10, and IFN-gamma have important and cross-regulatory roles in infection. In the past year, much progress has been made in the understanding of the cellular and molecular mechanisms involved in the regulation (and cross-regulation) of these three cytokines and their role in pathology. IL-12 is rapidly produced after infection and acts as a proinflammatory cytokine eliciting the production, by T cells and natural killer cells, of IFN-gamma which activates phagocytic cells. The production of IL-12 is strictly regulated by negative and positive feedback mechanisms. If IL-12 and IL-12-induced IFN-gamma are present during early T cell expansion in response to antigen, Th1 cell generation is favored and the generation of Th2 cells is inhibited. Thus, IL-12 is also a potent immunoregulatory cytokine which promotes Th1 differentiation and is instrumental in the Th1-dependent resistance to infections by bacteria, intracellular parasites, fungi, and certain viruses. Viruses inducing a permanent or transient immunodepression, such as HIV and measles, may act, in part, by suppressing IL-12 production.
白细胞介素-12（IL-12）、白细胞介素-10（IL-10）和γ干扰素（IFN-γ）这三种细胞因子在感染过程中发挥着重要的交叉调节作用。在过去的一年里，我们对这三种细胞因子的调节（以及交叉调节）所涉及的细胞和分子机制及其在病理学中的作用有了很大进展。感染后，IL-12迅速产生，并作为一种促炎细胞因子，促使T细胞和自然杀伤细胞产生IFN-γ，而IFN-γ可激活吞噬细胞。IL-12的产生受到正负反馈机制的严格调控。如果在抗原刺激下T细胞早期扩增过程中存在IL-12和IL-12诱导的IFN-γ，则有利于Th1细胞的生成，而抑制Th2细胞的生成。因此，IL-12也是一种强大的免疫调节细胞因子，可促进Th1分化，并在Th1依赖的抵抗细菌、细胞内寄生虫、真菌和某些病毒感染中发挥作用。诱导永久性或暂时性免疫抑制的病毒，如HIV和麻疹病毒，可能部分通过抑制IL-12的产生来发挥作用。
