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Thermal and Mountain Medicine Division, United States Army Research Institute of Environmental Medicine, Natick, Massachusetts 01760-5007
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-
(TNF-) 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.
interleukin-1; interleukin-6; interleukin-10; tumor necrosis factor; thermoregulation
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