Complement activation and inhibition in experimental models of arthritis

Mol Immunol. Sep-Oct 1999;36(13-14):905-14. doi: 10.1016/s0161-5890(99)00113-3.

Abstract

Complement activation has been implicated as a pathological process in a number of inflammatory and autoimmune disorders including chronic rheumatoid arthritis (RA). Animal models of experimental arthritis have been widely used to investigate the pathogenesis of RA and also in the development of novel therapies. Many of these models are complement-dependent and both incidence and progression of disease can be influenced by complement inhibition. In certain situations, local inhibition is of greater therapeutic benefit than systemic decomplementation. An increasing awareness and availability of a wide range of naturally occurring complement regulatory proteins can now offer a more targeted approach to complement inhibition while the availability of novel engineering strategies has also improved the efficiency of this process. The success of complement inhibition in the experimental models described should offer a novel therapeutic approach to the treatment of human inflammatory arthritis.

Publication types

  • Review

MeSH terms

  • Animals
  • Arthritis / drug therapy
  • Arthritis / etiology*
  • Arthritis / immunology*
  • Arthritis, Experimental / drug therapy
  • Arthritis, Experimental / etiology
  • Arthritis, Experimental / immunology
  • Arthritis, Rheumatoid / drug therapy
  • Arthritis, Rheumatoid / etiology
  • Arthritis, Rheumatoid / immunology
  • Bacteria / immunology
  • Cell Wall / immunology
  • Collagen / immunology
  • Complement Activation*
  • Complement Inactivator Proteins / pharmacology*
  • Disease Models, Animal
  • Elapid Venoms / pharmacology
  • Humans
  • Mice
  • Receptors, Complement 3b / metabolism

Substances

  • Complement Inactivator Proteins
  • Elapid Venoms
  • Receptors, Complement 3b
  • cobra venom factor
  • Collagen