The Progression of the Inflammation in Established Collagen-Induced Arthritis Can Be Altered by Treatments With Immunological or Pharmacological Agents Which Inhibit T Cell Activities

Eur J Immunol. 1988 Jun;18(6):881-8. doi: 10.1002/eji.1830180608.


Alterations in the progression of the inflammatory disease in mice with established collagen-induced arthritis (CIA) by in vivo treatments with either anti-T cell antibodies or an immunosuppressive drug, whose main targets of action are T cells, were studied. It was demonstrated that the in vivo administration of either monoclonal anti-L3T4, anti-Ly-2 or the combination of anti-L3T4 and anti-Ly-2 failed to modify the inflammatory disease after the arthritis had been initiated. Nevertheless, the progression of disease was decreased by treatments with rabbit anti-mouse lymphocyte sera (ALS) in mice with established CIA. While there was a substantial reduction in the proliferative responses to the T cell mitogen concanavalin A (Con A) in these ALS-treated mice, proliferation to a B cell mitogen, lipopolysaccharide, was unaffected. Furthermore, treatments with anti-Thy-1.2 monoclonal antibody (mAb) by itself did not alter the progression of the ongoing inflammatory disease, but combined treatments with both anti-Thy-1.2 and anti-L3T4 mAb prevented the further advancement of the arthritic disease. Although mice receiving either anti-Thy-1.2 alone or both anti-Thy-1.2 and anti-L3T4 exhibited complete absence of Thy-1+ cells within their inguinal lymph nodes, the proliferative responses to Con A by LN cells from mice treated with the combination of anti-Thy-1.2 and anti-L3T4 were drastically reduced compared to the responses of either the anti-Thy-1.2 or anti-L3T4-treated groups. Finally, daily treatments with cyclosporin A, an immunosuppressive drug which preferentially acts on T cells, were also effective in modifying the clinical course of the arthritic disease in mice with established CIA. These results suggest that immunocompetent cells which express the Thy-1 surface marker, most likely Thy-1+ T cells, may play a role in maintaining and perpetuating the inflammatory disease of established CIA.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / administration & dosage*
  • Anti-Inflammatory Agents / therapeutic use
  • Antibodies, Monoclonal / administration & dosage
  • Antibody Specificity
  • Antigens, Differentiation, T-Lymphocyte / immunology
  • Antilymphocyte Serum / administration & dosage
  • Arthritis / prevention & control*
  • Arthritis, Experimental / immunology
  • Arthritis, Experimental / pathology
  • Arthritis, Experimental / prevention & control*
  • Collagen
  • Cyclosporins / administration & dosage
  • Immunosuppressive Agents / administration & dosage*
  • Immunosuppressive Agents / therapeutic use
  • Male
  • Mice
  • Mice, Inbred DBA
  • T-Lymphocytes / classification
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology*


  • Anti-Inflammatory Agents
  • Antibodies, Monoclonal
  • Antigens, Differentiation, T-Lymphocyte
  • Antilymphocyte Serum
  • Cyclosporins
  • Immunosuppressive Agents
  • Collagen