Evolution of collagen arthritis in mice is arrested by treatment with anti-tumour necrosis factor (TNF) antibody or a recombinant soluble TNF receptor

Immunology. 1992 Dec;77(4):510-4.


Immunization of DBA/1 mice with type II collagen within complete Freund's adjuvant leads to arthritis, lasting more than 3 months. Injection of anti-tumour necrosis factor (TNF) IgG, 2 and 3 weeks after immunization prevented the development of arthritis in the following months. This treatment had no effect when started 2 months after induction of the disease. A soluble form of the human recombinant TNF receptor type-beta (rsTNFR-beta), continuously infused at a rate of 20 micrograms/day during the second and third week after immunization, also had a long-term protective effect. Anti-TNF antibody had no effect upon the production of anti-type II collagen antibodies. These results indicate that TNF is critically involved in an early phase of this arthritis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arthritis / immunology*
  • Arthritis / pathology
  • Arthritis / prevention & control
  • Autoantibodies / biosynthesis
  • Collagen / immunology*
  • Foot / pathology
  • Immunoglobulin G / immunology
  • Male
  • Mice
  • Mice, Inbred DBA
  • RNA, Messenger / analysis
  • Receptors, Cell Surface / immunology
  • Receptors, Tumor Necrosis Factor
  • Recombinant Proteins / immunology
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology*


  • Autoantibodies
  • Immunoglobulin G
  • RNA, Messenger
  • Receptors, Cell Surface
  • Receptors, Tumor Necrosis Factor
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Collagen