If you are asking about cellular mechanism in the hypothalamus, see below.

From: https://www.ncbi.nlm.nih.gov/books/NBK562334/

Milton and Wendlandt demonstrated that fever is mediated by the pyrogenic activity of prostaglandins (PGs), specifically PGE2. The synthesis of PGE2 begins with membrane phospholipids being converted to arachidonic acid (AA) by phospholipase A2 (PLA2). AA is then converted to PGH2 via cyclooxygenase (COX), after which PGH2 undergoes isomerization to PGE2 by PGE synthase. PGE2 acts via the EP3 receptor to affect specific neurons within the hypothalamus that aid in thermoregulation. Medications that inhibit COX are a mainstay of treatment for fevers, as it halts the conversion of AA into PGE2 and, thus, other prostanoids that can lead to fever.

The action of PGE2 begins when exogenous pyrogens (e.g., bacteria, viruses) stimulate endogenous pyrogens such as IL-1, IL-6, tumor necrosis factor (TNF), and interferon (IFN) to alter the hypothalamic set point via the organum vasculosum of the lamina terminalis (OVLT) and raise the core body temperature. Endogenous pyrogens also act to trigger an immune and inflammatory response. The immune response includes leukocytosis, T cell activation, B cell proliferation, NK cell killing, and increased white blood cell adhesion. The inflammatory response includes increased acute phase reactants, increased muscle protein breakdown, and increased synthesis of collagen.[4]