Taylor C G, Giesbrecht J A
Department of Foods and Nutrition, University of Manitoba, Winnipeg, Canada.
Can J Physiol Pharmacol. 2000 Oct;78(10):823-8.
Impaired immune function in dietary zinc (Zn) deficiency is characterized in part by reduced lymphocyte numbers (lymphopenia) and depressed cell-mediated (T lymphocyte) immune function, however, the causative mechanisms at the molecular level have not been elucidated. This paper will focus on the role of dietary Zn in T lymphocyte signal transduction, and specifically, the early Zn-dependent steps for phosphorylation and the putative Zn-finger proteins or Zn-metalloenzymes that may be part of the molecular mechanism for explaining immune dysfunction in Zn deficiency. One of the major recent findings is that murine splenic T lymphocyte p56lck expression is elevated in dietary Zn deficiency and caloric deficiency. Based on the known functions of p56lck, it is proposed that elevated p56lck may contribute to altered thymocyte maturation, apoptosis, and lymphopenia in dietary Zn deficiency and other malnutrition syndromes.
饮食中锌（Zn）缺乏导致的免疫功能受损部分表现为淋巴细胞数量减少（淋巴细胞减少）和细胞介导的（T淋巴细胞）免疫功能低下，然而，分子水平上的致病机制尚未阐明。本文将重点关注饮食中锌在T淋巴细胞信号转导中的作用，特别是早期锌依赖性磷酸化步骤以及可能是解释锌缺乏时免疫功能障碍分子机制一部分的假定锌指蛋白或锌金属酶。最近的一项主要发现是，在饮食锌缺乏和热量缺乏的情况下，小鼠脾脏T淋巴细胞p56lck表达升高。基于p56lck的已知功能，有人提出p56lck升高可能导致饮食锌缺乏和其他营养不良综合征中胸腺细胞成熟改变、细胞凋亡和淋巴细胞减少。
