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From the Department of Experimental Pathology, Scripps Clinic and Research Foundation, 476 Prospect Street, La Jolla, California 92037
Abstract
The influence of complement components upon the movement of neutrophils and development of immunologic injury was tested in immune complex injury of rabbit synovial tissue. Suspensions of purified neutrophils were infused in the joint space of rabbits depleted of neutrophils which were prepared for a reversed passive Arthus reaction in the synovial tissues. The neutrophils migrated through the tissues to the site of antigen-antibody-complement deposition in the walls of blood vessels. Injury followed the accumulation of neutrophils in the vessel walls and was assessed by leakage of radiolabeled proteins from the circulation into the joint space, deposition of carbon black from the circulation into the area of the injured vessel and diapedesis of red blood cells. Animals genetically deficient in C6 or depleted of C3 with cobra venom factor showed a retarded rate of neutrophil migration through the synovial tissues to the site of antigen-antibody complex. Injury was delayed and diminished in the rabbits deficient in complement. The results indicate the presence of complement dependent chemotaxis in vivo. They also demonstrate the reconstitution of immunologic injury in neutrophil depleted animals by the replacement of purified neutrophils.
Footnotes
1 Publication No. 555 from the Department of Experimental Pathology, Scripps Clinic and Research Foundation, 476 Prospect Street, La Jolla, California 92037. The work was supported by United States Public Health Service Grant AI-07007, The National Multiple Sclerosis Society Grant 459 and The Council for Tobacco Research, USA (#764).
2 Post-doctoral Fellow supported by United States Public Health Service Graduate Training Grant in Surgery, 5 T01 GM 173346. Present address: Department of Surgery, The University of Texas, Southwestern Medical School at Dallas, Dallas, Texas 75235.
3 Recipient of Research Career Development Award 5 K04 GM 42567-02.
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