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Immunopathologic Studies in Relapsing Polychondritis

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Immunopathologic Studies in Relapsing Polychondritis Immunopathologic Studies in Relapsing Polychondritis Jerome H. Herman, Marie V. Dennis J Clin Invest. 1973;52(3):549-558. https://doi.org/10.1172/JCI107215. Research Article Serial studies have been performed on three patients with relapsing polychondritis in an attempt to define a potential immunopathologic role for degradation constituents of cartilage in the causation and/or perpetuation of the inflammation observed. Crude proteoglycan preparations derived by disruptive and differential centrifugation techniques from human costal cartilage, intact chondrocytes grown as monolayers, their homogenates and products of synthesis provided antigenic material for investigation. Circulating antibody to such antigens could not be detected by immunodiffusion, hemagglutination, immunofluorescence or complement mediated chondrocyte cytotoxicity as assessed by 51Cr release. Similarly, radiolabeled incorporation studies attempting to detect de novo synthesis of such antibody by circulating peripheral blood lymphocytes as assessed by radioimmunodiffusion, immune absorption to neuraminidase treated and untreated chondrocytes and immune coprecipitation were negative. Delayed hypersensitivity to cartilage constituents was studied by peripheral lymphocyte transformation employing [3H]thymidine incorporation and the release of macrophage aggregation factor. Positive results were obtained which correlated with periods of overt disease activity. Similar results were observed in patients with classical rheumatoid arthritis manifesting destructive articular changes. This study suggests that cartilage antigenic components may facilitate perpetuation of cartilage inflammation by cellular immune mechanisms. Find the latest version: https://jci.me/107215/pdf Immunopathologic Studies in Relapsing Polychondritis JERoME H. HERmAN and MARIE V. DENNIS From the Division of Immunology, Department of Internal Medicine, University of Cincinnati Medical Center, Cincinnati, Ohio 45229 A B S T R A C T Serial studies have been performed on as hematologic and serologic disturbances. There is three patients with relapsing polychondritis in an at- little insight into etiologic or pathophysiologic factors tempt to define a potential immunopathologic role for operative in this disease. A pathologic similarity has degradation constituents of cartilage in the causation been shown to exist between polychondritis and the ex- and/or perpetuation of the inflammation observed. Crude perimental papain (1) and hypervitaminosis-A (2) in- proteoglycan preparations derived by disruptive and duced depletion of cartilaginous matrix as well as the differential centrifugation techniques from human costal model of complement-dependent cartilage lysis in vitro, cartilage, intact chondrocytes grown as monolayers, mediated by anti-cell membrane antibody (3, 4). How- their homogenates and products of synthesis provided ever, the inflammation with predominant round cell antigenic material for investigation. Circulating antibody infiltration and degeneration of chondrocytes observed to such antigens could not be detected by immunodiffu- in polychondritis are conspicuous differences. sion, hemagglutination, immunofluorescence or comple- It is of interest that diseases such as rheumatoid arth- ment mediated chondrocyte cytotoxicity as assessed by ritis, Sjdgren's syndrome, and lupus errthematosus in 'Cr release. Similarly, radiolabeled incorporation stud- which immunologic events appear to play a significant ies attempting to detect de novo synthesis of such anti- role in the mediation of inflammation may coexist with body by circulating peripheral blood lymphocytes as as- polychondritis. However, other than an inconclusive re- sessed by radioimmunodiffusion, immune absorption to port by Dolan, Lemmon, and Teitelbaum (5), there neuraminidase treated and untreated chondrocytes and has been no apparent attempt to incriminate such im- immune coprecipitation were negative. munopathologic events in the pathogenesis of this disease. Delayed hypersensitivity to cartilage constituents was In the present report, serial immunologic studies per- studied by peripheral lymphocyte transformation em- formed on three patients with polychondritis are presented ploying [3H]thymidine incorporation and the release of in an attempt to define potential mechanisms operative in macrophage aggregation factor. Positive results were the causation and/or perpetuation of the cartilage inflam- obtained which correlated with periods of overt disease mation observed. activity. Similar results were observed in patients with classical rheumatoid arthritis manifesting destructive METHODS articular changes. This study suggests that cartilage Cartilage antigen preparation. Human cartilage antigens antigenic components may facilitate perpetuation of car- were derived from two sources. The method of Malawista and Schubert (6) employing water extraction with high tilage inflammation by cellular immune mechanisms. speed homogenization was utilized to secure crude proteo- glycan (PG)' from human costal cartilage. Protein poly- saccharide light (PP-L) and heavy (PP-H) derivatives INTRODUCTION were prepared as described by Gerber, Franklin, and Schu- Relapsing polychondritis is a relatively rare disorder bert (7) based upon differential centrifugation of PG. Chondrocytes, asepticaly isolated from human articular characterized by prominent inflammation of cartilagenous cartilage by collagenase digestion (8) were maintained in structures. Though cartilage inflammation predominates, monolayer culture employing Eagle's minimum essential one may observe ocular and cardiac involvement as well medium 2 containing 20% fetal calf serum, l-glutamine, peni- This work was presented in part at the American Rheu- 1Abbreviations used in this paper: ANA, antinuclear anti- matism Association meeting, Washington, D. C., January body; MCP, metacarpophalangeal joints; PG, proteoglycan; 1971. (1971. Arthritis Rheum. 14: 166.) PHA, phytohemagglutinin; PIP, proximal interphalangeal Dr. Herman is a Post-Doctoral Fellow of the Arthritis joints; PP-H, protein polysaccharide heavy derivatives; Foundation. PP-L, protein polysaccharide light derivatives; SCAT, Received for publication 1 August 1972 and in revised sheep cell agglutination tests; TCA, trichloroacetic acid. form 24 October 1972. 'Grand Island Biological Co., Grand Island, N. Y. The Journal of Clinical Investigation Volume 52 March 1973 549 cillin, streptomycin, and mycostatin. Subculturing was un- phosphate-buffered saline, the original supernates and washes dertaken as necessary. Studies were performed upon intact were pooled, and a portion was removed for scintillation chondrocytes, their mechanical homogenates and products of counting. Pellets were dissolved in 0.5NaOH and suspended chondrocyte synthesis derived from ultrafiltration of growth in Bray's phosphor, and liquid scintillation counting was media at time of biweekly change. performed. Percentage of counts binding to chondrocytes Cartilage antibody preparation. Anti-proteoglycan (anti- was compared with counts originally added to the culture PG) antisera was obtained by hyperimmunizing rabbits to system as well as those recovered in supernatant portions. PG and PP-L, both of which had been pretreated with hy- Antibody-mediated cytotoxicity experiments were per- aluronidase' (9) and incorporated into complete Freund's formed in which chondrocytes, labeled with sodium chro- adjuvant. Antisera was concentrated by 40% ammonium mate, "Cr (5.0 gg/1 ml) ,7 were incubated with decomple- sulfate precipitation and repeatedly absorbed with lyophi- mented polychondritis or control sera in the presence of lized normal human serum and hyaluronidase. By immuno- fresh rabbit complement. Appropriate volumes of the 5'Cr electrophoresis, these antisera produced two lines on reac- solution were added to the cell suspension to give a final tion with hyaluronidase treated PG and PP-L as has been radioactive level of 25 uCi/3 ml at a cell concentration of reported previously (10). When reacted by immunodiffusion 106 cells/ml. Cytotoxicity was assessed by determining iso- with the chondrocyte culture media concentrate, a single tope release after a 1 h incubation at 37'C. A Packard line resulted indicating the ability of these cells to synthe- gamma scintillation system was employed (Packard Instru- size PG. ment Co., Inc., Downers Grove, Ill.). IDectection of anti-cartilage antibody. Several techniques Chondrocyte DNA synthesis. To further determine the were employed in an attempt to detect circulating antibody role of humoral factors, the DNA synthesizing capacity of to cartilage constituents in serial serum specimens from chondrocytes in suspension culture was determined by pulse the polychondritis patients. Immunodiffusion and tanned cell labeling for 16 h with [3H]thymidine' (sp. act. 11 Ci/mmol) hemagglutination studies were performed employing hyalu- in the presence of decomplemented polychondritis or normal ronidase-treated and untreated cartilage antigen prepara- sera substituted for fetal calf serum in the growth media tions (9). Indirect immunofluorescent techniques were un- 48 h previously. Upon termination of the experiments, the dertaken utilizing both fixed and viable chondrocytes as a cell button was pelleted by centrifuging at 150 g, DNA ex- source of antigen. Slides were read on a AO Fluorolume tracted, and liquid scintillation counting performed utilizing fluorescent microscope' using BG-12 and Corning no. 5113 a toluene phosphor (13). In
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