The main pathological feature of inflammation consists of leukocyte infiltration and exudation of plasma into the lesion in the early stage followed by proliferation of connective tissue including fibroblasts, which leads to the formation of granulation tissue. Systemic manifestations include elevation of body temperature and increase of serum acute phase reactants such as C-reactive protein and serum amyloid A. Most of these reactions are presumed to be caused by mediators which are produced by a various kinds of cells and tissues upon contact with inflammatory stimuli, such as bacteria, helminths, viruses, etc. Recently, it has become known that most of inflammatory stimuli induce the production of large amounts of several cytokines including interleukin 1 (IL-1), IL-6, and tumor necrosis factor (TNF) alpha and that these cytokines exert a wide variety of effects to accelerate inflammation. Hence, these cytokines are called "pro-inflammatory cytokines". These cytokines have overlapping biological functions and induce the production of each other, thus forming a complicated cytokine network. Here, in order to review the roles of these cytokines in the progression of inflammation, the effects on the body temperature, leukocyte infiltration and production of serum acute phase reactants, in particular, will be discussed.