Lefkowith J B
Div. of Rheumatology, Washington University School of Medicine, St. Louis, MO 63110.
Adv Prostaglandin Thromboxane Leukot Res. 1990;20:224-31.
EFA deficiency appears to be a uniquely useful tool in probing the role of arachidonate in a variety of physiologic and pathologic processes. Recent studies have clarified the effects of the deficiency state on tissue fatty acid content and on the production of metabolites of arachidonate and related mediators such as PAF. The ability of EFA deficiency to ameliorate a variety of inflammatory states, particularly models of autoimmune disease, is striking. The central mechanism appears to be the ability of EFA deficiency to inhibit leukocyte migration into foci of inflammation. The mechanisms underlying this phenomenon are currently under investigation. Additionally EFA deficiency has the capacity to alter dramatically tissue immunogenicity by affecting the representation of Ia-bearing cells within tissues. The role of arachidonate in the regulation of Ia-bearing cells within tissues is an area of continuing interest.
必需脂肪酸缺乏似乎是探究花生四烯酸在各种生理和病理过程中作用的一种特别有用的工具。最近的研究已经阐明了缺乏状态对组织脂肪酸含量以及花生四烯酸代谢产物和相关介质（如血小板活化因子）产生的影响。必需脂肪酸缺乏改善多种炎症状态的能力，尤其是自身免疫性疾病模型，令人瞩目。其核心机制似乎是必需脂肪酸缺乏抑制白细胞迁移到炎症病灶的能力。这种现象背后的机制目前正在研究中。此外，必需脂肪酸缺乏能够通过影响组织内Ia阳性细胞的表现来显著改变组织免疫原性。花生四烯酸在组织内Ia阳性细胞调节中的作用是一个持续受到关注的领域。
