The removal of aggregated and nonaggregated autologous gamma globulin from rheumatoid joints

Sliwinski, Anthony J.; Zvaifler, Nathan J.

doi:10.1002/art.1780120507

Cited by 22 publications

(11 citation statements)

References 16 publications

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“…As reported previously (13), RISA clearance in RA effusions (0.071 t 0.028 ml/minute) was significantly greater than that o. 8 found in OA effusions (0.039 k 0.030 ml/minute). Iodide clearance in RA effusions (1.92 t 0.30 ml/minute) was similar to that observed in OA effusions (2.19 t 0.52 ml/minute).…”

Section: Resultssupporting

confidence: 83%

Protein traffic in human synovial effusions

Wallis

Simkin

Nelp

1987

Arthritis & Rheumatism

125

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Concentrations of 5 marker proteins were measured in synovial fluid and serum samples from knee effusions of 11 patients with rheumatoid arthritis and 9 with osteoarthritis. Indirect determinations of synovial plasma flow and lymphatic drainage were obtained by measuring iodide clearance (mVminute) and radioalbumin clearance (mYminute). Together with protein concentrations, these determinations allowed us to calculate: 1) the flux of each marker protein through synovial tissues (mghinute); 2) the volume of plasma cleared by synovium per unit time (mlhinute); and 3) the fractional extraction per passage through the synovial microcirculation (protein permeance). These measures differed substantially between rheumatoid arthritis and osteoarthritis patient populations and quantified the severity of the microvascular lesion in rheumatoid synovitis.Synovial microvascular permeability plays an important role in the pathophysiology of synovial effusions. Permeability changes, however, have not been easily quantified. Previous evaluations assayed marker proteins in synovial fluid (SF) and serum (S) and then used the concentration ratio (SF:S) to charFrom the Departments of Medicine and Radiology, University of Washington, Seattle.Supported in part by NIH grants AM-22186, AM-32811, AM-07108, and RR-37, and by a Clinical Research Center grant from the Arthritis Foundation.acterize the "leakiness" of the synovial tissue barrier (1,2). Such studies provided support for the view that rheumatoid synovial tissues are more permeable than are osteoarthritic synovial tissues. The regression lines created by plotting SF:S versus protein molecular size have also been useful in determining whether specific proteins are consumed or synthesized within the articular compartment (1-3).Unfortunately, SF:S protein ratios reflect not only the permeability of synovial microvessels, but also the kinetics of plasma delivery to and lymphatic removal from synovial tissues. The contributions of these kinetic factors must be resolved in order to specifically assess microvascular permeability. In addition, net intraarticular synthesis or catabolism must be considered (4). Since the SF:S ratio fails to distinguish the several factors contributing to protein delivery and removal, it remains an inadequate measure of synovial microvascular permeability (5).Evidence from studies of animals indicates that protein traffic across the synovium is unidirectional, with proteins delivered to articular tissues by the microcirculation and removed by lymphatic drainage (6,7). Three groups of investigators have found that radiolabeled proteins of widely different molecular radius are removed from human articular tissues at identical rates (8-10). A shared rate suggests that proteins are not cleared by diffusion (in which case, the removal of different proteins would be inversely drainage.We have recently introduced a method for deriving the articular clearance of radiolabeled albumin (RISA) from human synovial effusions (11). Be-98195.

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Section: Resultssupporting

confidence: 83%

Protein traffic in human synovial effusions

Wallis

Simkin

Nelp

1987

Arthritis & Rheumatism

125

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“…The development of these reversed Arthus lesions canl be explained by the fact that when a solution is injected into the joint space it enters the circulation through venules in the synovium (22 (25). Their studies showed a similar rate of loss of albumiiin and TgG from the knee joint.…”

Section: Development Of Immunologic Injury In the Synoviummentioning

confidence: 97%

“…3d). For control studies rabbit blood was separated into erythrocyte, mononuclear cell, neutrophil, and platelet fractions (the latter in a concentration 25 times that contaminating the usual neutrophil preparation). Portions of each component were introduced into different joints, but only the neutrophils produced (Fig.…”

Section: Development Of Immunologic Injury In the Synoviummentioning

confidence: 99%

Acute Immunologic Arthritis in Rabbits

DeShazo¹,

Henson²,

Cochrane³

1972

J. Clin. Invest.

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A B S T R A C T Mediators of acute immunologic injury have been studied in vivo by producing arthritis in rabbit knee joints. A reversed passive Arthus lesion was produced by injecting antibody into the joint space and antigen intravenously. Injury was assessed by measuring leakage of serumii proteins and circulating radiolabeled proteins into the joint space and by the accumulation of neutrophils in the joint fluid. Inflammatory exudate was recovered for study by a standardized irrigation technique.Maximal vascular permeability developed 2 hr after injection as neutrophils accumulated about immune complexes in venule walls to produce structural injury. After 5 hr the number of neutrophils in the joint space rose rapidly, followed by a second rise in permeability at 8 hr. Neutrophil depletion abolished both peaks of permeability. It was then possible to reconstitute the synovial lesion in neutrophil-depleted rabbits by intraarticular injection of purified suspensions of neutrophils.A requirement for complement was demonstrated in development of the lesion. Rabbits genetically deficient in C6 showed delay in vascular permeability, appearance of neutrophils, and histologic lesions. The delay was longer in normal rabbits depleted of C3. In C6-deficient rabbits depleted of C3, still further reduction in injury occurred.Evidence was obtained as well for a chemotactic attraction of neutrophils in vivo. Antigen-antibody-complement complexes in the walls of blood vessels attracted neutrophils placed in the joint space of neutrophil-depleted rabbits. Omission of either antigen or antibody from this replacement reaction prevented the migration of neutrophils.

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“…Though the exper.iments of Hollander and his collaborators (1, 2) (who found that injection of autologous IgG into quiescent joints could produce exacerbations of synovitis) were interpreted on the basis of an immune complex reaction between injected IgG and RF, this work has not been successfully repeated (3). Davis has postulated that RF may actually inhibit inflammation produced by immune complexes (4).…”

Section: Introductionmentioning

confidence: 99%

Effect of Rheumatoid Factor on Complement-Mediated Phagocytosis

McDuffie¹,

Brumfield²

1972

J. Clin. Invest.

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Foundation, Rochester Minnesota 55901 A B S T R A C T The frequency and amount of IgM rheumatoid factor (RF) in the blood of patients with rheumatoid arthritis (RA) correlate with the severity of the disease and the number of complications. Though previous studies of RF in subacute bacterial endocarditis have shown that RF inhibits phagocytosis of microorganisms by granulocytes, the presence of low levels of complement (C) in blood and synovial fluid of patients with the highest titers of RF suggests that an interaction between RF and C may contribute to the -inflammatory process in RA. We thus employed a quantitative methodology to examine the effect of RF on complement-dependent phagocytosis of sheep erythrocytes by rabbit granulocytes. Addition of 2500 molecules of IgM RF to sheep cells heavily coated with IgG antibody (195,000 molecules per cell) resulted in virtually complete inhibition of uptake of C3 (flue) and prevention of phagocytosis, an effect resulting from inhibition of uptake of Cl by the cells. When erythrocytes coated with only 34,000 molecules of IgG antibody were employed, phagocytosis was similarly inhib.ited. However the effect of RF on such cells was shown to be primarily mediated through inhibition of C4 rather than Cl uptake. Although the results do not exclude the participation of an

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The removal of aggregated and nonaggregated autologous gamma globulin from rheumatoid joints

Cited by 22 publications

References 16 publications

Protein traffic in human synovial effusions

Protein traffic in human synovial effusions

Acute Immunologic Arthritis in Rabbits

Effect of Rheumatoid Factor on Complement-Mediated Phagocytosis

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