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- Title
Anti-neutrophil monoclonal antibody therapy inhibits the development of adjuvant arthritis.
- Authors
Santos, L. L.; Morand, E. F.; Hutchinson, P.; Boyce, N. W.; Holdsworth, S. R.
- Abstract
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 loukocylosis associated with AA (3.3 ± 0.6 × 10³/mm³ versus 21.2 ± 6.9 × 10³/mm³ P<0.001). On day 12, control animals exhibited severe arthritis as assessed by articular index (Al) (9.2 ± 1.3), increase in paw volume (149.3 ± 10.6%), and synovial fluid (SF) cell count (5.3 ± 0.5 × 105). RP3 treatment significantly reduced Al (1 ± 0.1; P<0 .001), paw volume (103.6±5.8%; P <0.001) and SF cells (0.6 ± 0.l × l05; 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 Icuctxryte influx in AA. suggesting a pivotal role for neutrophils in the effector phase of AA. Inhibition of neutrophil accumulation by CD4+ cell depiction and not by decomplementation suggests that neutrophil accumulation in AA is T cell-dependent.
- Subjects
NEUTROPHILS; RHEUMATOID arthritis; IMMUNOLOGICAL adjuvants; MONOCLONAL antibodies; MYCOBACTERIUM tuberculosis; T cells; LABORATORY rats
- Publication
Clinical & Experimental Immunology, 1997, Vol 107, Issue 2, p248
- ISSN
0009-9104
- Publication type
Article
- DOI
10.1111/j.1365-2249.1997.263-ce1154.x