Molecular biology of thermoregulation - Invited review: Cytokine regulation of fever: studies using gene knockout mice
Molecular biology of thermoregulation - Invited review: Cytokine regulation of fever: studies using gene knockout mice
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DOI：
10.1152/japplphysiol.01005.2001
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发表时间：
2002-06-01
影响因子：
3.3
通讯作者：
Leon, LR
中科院分区：
文献类型：
--
作者：
Leon, LR
发烧被定义为体温的有规律的升高。这种现象的调节是通过两种内源性细胞因子的作用来完成的，一些细胞因子充当热原，另一些充当解热剂。先前通过使用传统药理学技术（例如注射中和抗体）获得的数据表明白细胞介素（IL）-1和IL-6是内源性热原或发烧诱导剂。几乎在所有 IL-1 或 IL-6 的内源性作用被拮抗的情况下，发烧都会减弱。其他细胞因子，例如肿瘤坏死因子-α (TNF-α) 和 IL-10，被认为具有内源性退热剂或发烧抑制剂的作用。在一些研究中，TNF 作用的抑制会加剧发烧。最近，通过基因工程使全身所有组织中缺乏细胞因子或其受体的小鼠已被用来检查 IL-1、IL-6、TNF 和 IL-10 对发烧的调节作用。从这些小鼠身上获得的数据为我们对发烧时细胞因子相互作用的理解提供了新的线索，并且在某些情况下与药理学方法获得的数据相矛盾。本综述总结了细胞因子和细胞因子受体敲除小鼠对脂多糖、松节油和脓毒症引起的发烧的反应。
Fever is defined as a regulated rise in body temperature. The regulation of this phenomenon is accomplished by the actions of two types of endogenous cytokines, some functioning as pyrogens and others as antipyretics. Previous data obtained with the use of traditional pharmacological techniques, such as the injection of neutralizing antibodies, implicate interleukin (IL)-1 and IL-6 as endogenous pyrogens or inducers of fever. In almost all instances in which the endogenous actions of IL-1 or IL-6 are antagonized, fevers are attenuated. Other cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and IL-10, are thought to act as endogenous antipyretics or inhibitors of fever. In several studies, the inhibition of TNF action has enhanced fever. Recently, mice genetically engineered to lack cytokines or their receptors in all tissues of the body have been used to examine the regulation of IL-1, IL-6, TNF, and IL-10 on fever. Data obtained with these mice shed new light on our understanding of cytokine interactions in fever and, in some instances, contradict data obtained with pharmacological methods. This review summarizes the responses of cytokine and cytokine receptor knockout mice to fevers induced by lipopolysaccharide, turpentine, and sepsis.