Anti-neutrophil monoclonal antibody therapy inhibits the development of adjuvant arthritis

Clin Exp Immunol. 1997 Feb;107(2):248-53. doi: 10.1111/j.1365-2249.1997.263-ce1154.x.


The aim of this study was to determine the contribution of neutrophils to adjuvant arthritis (AA) by in vivo depletion of peripheral blood neutrophils. Specific anti-neutrophil MoAb, RP3 (10 mg), or a control antibody was given twice daily on days 8-11 after injection of Mycobacterium tuberculosis in inbred male Sprague-Dawley rats. RP3 treatment inhibited the neutrophil leukocytosis associated with AA (3.3 +/- 0.6 x 10(3)/mm3 versus 21.2 +/- 6.9 x 10(3)/mm3; P<0.001). On day 12, control animals exhibited severe arthritis as assessed by articular index (AI) (9.2 +/- 1.3), increase in paw volume (149.3 +/- 10.6%), and synovial fluid (SF) cell count (5.3 +/- 0.5 x 10(5)). RP3 treatment significantly reduced AI (1 +/- 0.1; P<0.001), paw volume (103.6 +/- 5.8%; P<0.001) and SF cells (0.6 +/- 0.1 x 10(5); P<0.001) without affecting cutaneous DTH (treated 0.6 +/- 0.1 mm change in thickness, control 0.8 +/- 0.2 mm; NS). Additional experiments demonstrated that CD4+ cell depletion but not decomplementation inhibited AA development and synovial neutrophil accumulation. Depletion of circulating neutrophils prevented joint inflammation and synovial leucocyte influx in AA, suggesting a pivotal role for neutrophils in the effector phase of AA. Inhibition of neutrophil accumulation by CD4+ cell depletion and not by decomplementation suggests that neutrophil accumulation in AA is T cell-dependent.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / therapeutic use*
  • Arthritis, Experimental / prevention & control*
  • Hypersensitivity, Delayed / therapy
  • Male
  • Neutrophils / immunology*
  • Rats
  • Rats, Sprague-Dawley
  • Skin / immunology


  • Antibodies, Monoclonal