Cytokines constitute an ever growing family of highly potent biological mediators. Our advanced knowledge of the molecular structure of most cytokines, their target receptors, and the respective coding genes contrasts with the still incomplete data available on physiological and pathophysiological regulatory mechanisms operating within the cytokine network. This explains the interest in studying in vivo situations, either in the clinic or in experimental models, where cytokines are directly implicated in the induction of profound sickness or tissue damage. Stimuli described as promoters of monocyte/macrophage or lymphocyte activation, leading to local or systemic cytokine release and pathology, are toxic silicosis (Piguet et al. 1990), bleomycin pneumopathy (Piguet et al. 1989), infectious bacterial endotoxin (Barnett-Sultzer 1968; Skidmore et al. 1975), tuberculosis (Kindler et al. 1989), malaria (Grau et al. 1990), leishmaniosis (Heinzel et al. 1989), or immunological conditions such as graft vs host disease (Piguet et al. 1989b).