Bernhagen J, Calandra T, Bucala R
Laboratory of Biochemistry, Interfacial Engineering, University of Stuttgart, Germany.
J Mol Med (Berl). 1998 Mar;76(3-4):151-61. doi: 10.1007/s001090050204.
The classical T cell cytokine macrophage migration inhibitory factor (MIF) has reemerged recently as a critical mediator of the host immune and stress response. MIF has been found to be a mediator of several diseases including gram-negative septic shock and delayed-type hypersensitivity reactions. Its immunological functions include the modulation of the host macrophage and T and B cell response. In contrast to other known cytokines, MIF production is induced rather than suppressed by glucocorticoids, and MIF has been found to override the immunosuppressive effects of glucocorticoids. Recently, elucidation of the three-dimensional structure of MIF revealed that MIF has a novel, unique cytokine structure. Here the biological role of MIF is reviewed in view of its distinct immunological and structural properties.
经典的T细胞细胞因子巨噬细胞移动抑制因子（MIF）最近再度成为宿主免疫和应激反应的关键介质。MIF已被发现是包括革兰氏阴性败血症性休克和迟发型超敏反应在内的多种疾病的介质。其免疫功能包括调节宿主巨噬细胞以及T细胞和B细胞反应。与其他已知细胞因子不同，MIF的产生是由糖皮质激素诱导而非抑制的，并且已发现MIF能抵消糖皮质激素的免疫抑制作用。最近，对MIF三维结构的阐明揭示了MIF具有一种新颖独特的细胞因子结构。在此，鉴于MIF独特的免疫学和结构特性，对其生物学作用进行综述。
