Fever is induced by interactions of bacterial pyrogens with cells from the immune system, which subsequently release a cascade of cytokines. After intramuscular injection of lipopolysaccharide (LPS) from E. coli, increased amounts of tumor necrosis factor (TNF) and interleukin-6 (IL-6) can be measured in blood plasma and in perfusates of the anterior hypothalamus, where body temperature is regulated. These substances are therefore candidates to be involved in the modification of thermoregulatory structures leading to the febrile rise in body temperature. This increase of body temperature is limited and sometimes even prevented by the actions of endogenous antipyretic neuropeptides like arginine vasopressin (AVP), adrenocorticotropin (ACTH) and melanocyte-stimulating hormones (MSHs) liberated within the brain or systemically during fever. For AVP, most experimental evidence confirms antipyretic pathways from the hypothalamic paraventricular nucleus to the septal area of the limbic system, which are activated during fever and by several stressful stimuli. Fever and endogenous antipyresis are interconnected and result from interactions between the immune system and the central nervous system.