Fever as a reset thermostat, not a malfunction
The hypothalamus holds a body temperature set-point much like a thermostat holds a target temperature. In fever, that target is deliberately raised. Until the body reaches the new higher target, a person feels cold and shivers and constricts blood vessels to generate and conserve heat, which is why chills often precede a measured temperature rise.
This is a regulated change, not a loss of control like heatstroke. When the set-point falls back to normal, the same machinery runs in reverse: sweating and vasodilation shed the extra heat.
The signaling chain from cytokine to PGE2
Pyrogenic cytokines including IL-1, IL-6, and TNF rise during infection. Acting at the brain's vascular interface, they drive production of prostaglandin E2 (PGE2), which acts on hypothalamic neurons to raise the set-point. Antipyretic drugs such as aspirin and other NSAIDs work largely by inhibiting the cyclooxygenase enzymes that make PGE2, which is why they lower fever.
Fever is generally an adaptive response, but very high or prolonged fever, fever in infants, or fever with serious symptoms warrants prompt medical evaluation. This is general educational information, not medical advice, and any decision about fever-reducing medication should involve a qualified professional.