title: Inhibiting the effects of cytokines in human diseases.
abstract: In reviewing some of the mechanisms whereby cytokine effects are inhibited or blocked, this chapter has illustrated that the cytokine network is truly self-regulating. Exaggerated effects of particular cytokines in disease processes may be due to unregulated production of proinflammatory cytokines or inadequate production of anti-inflammatory cytokines. In addition, cytokine effects may be regulated at the levels of production, protein binding, receptor expression, soluble receptor generation, or receptor binding. Monoclonal antibodies to TNF-alpha, soluble receptors for IL-1 or TNF, and IL-1ra represent four promising approaches for therapeutic intervention in human diseases. As more knowledge is gained about the cytokine network in human diseases, additional avenues for treatment through inhibition of cytokine effects are certain to evolve.
authors.affiliation: Division of Rheumatology, University of Colorado School of Medicine, Denver, USA.
authors.forename: W P
authors.initials: WP
authors.lastname: Arend
mesh_terms: D000818:Animals; D000906:Antibodies; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000276:immunology / Q000502:physiology; D005260:Female; D006801:Humans; D007378:Interleukins / Q000276:immunology; D008297:Male; D018123:Receptors, Interleukin; D018124:Receptors, Tumor Necrosis Factor; D016212:Transforming Growth Factor beta / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D000906:Antibodies; D016207:Cytokines; D007378:Interleukins; D018123:Receptors, Interleukin; D018124:Receptors, Tumor Necrosis Factor; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha