Interleukin-1 and Tumor Necrosis Factor: Effector Cytokines in Autoimmune Diseases

Semin Immunol. 1992 Jun;4(3):133-45.

Abstract

Autoimmune diseases have been studied from the perspective of an abnormal immune response in genetically vulnerable hosts. Although the immune response is responsible for the initiation of autoimmune diseases, the effectors of the disease process likely involves cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). These polypeptides induce a wide variety of inflammatory events which contribute to the destruction of tissue and tissue remodeling in several autoimmune diseases. Blocking IL-1 with its naturally occurring receptor antagonist, the IL-1 receptor antagonist reduces the severity of disease in animal models of inflammation and autoimmune processes. Clinical studies with the IL-1 receptor antagonist will define the role for this cytokine in the pathogenesis of autoimmune diseases such as arthritis, inflammatory bowel disease, type I diabetes and vasculitis.

Publication types

  • Comparative Study
  • Review

MeSH terms

  • Animals
  • Autoimmune Diseases / physiopathology*
  • Cytokines / physiology
  • Gene Expression Regulation*
  • Humans
  • Inflammation
  • Interleukin-1 / antagonists & inhibitors
  • Interleukin-1 / immunology
  • Interleukin-1 / physiology*
  • Interleukin-1 / toxicity
  • Interleukin-6 / physiology
  • Receptors, Cell Surface / physiology
  • Receptors, Immunologic / physiology
  • Receptors, Interleukin-1
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha / physiology*
  • Tumor Necrosis Factor-alpha / toxicity

Substances

  • Cytokines
  • Interleukin-1
  • Interleukin-6
  • Receptors, Cell Surface
  • Receptors, Immunologic
  • Receptors, Interleukin-1
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha