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1.  Antigens related to the major internal protein, p27, of a psoriasis associated retrovirus-like particle are expressed in patients with chronic arthritis. 
Annals of the Rheumatic Diseases  1985;44(11):761-765.
A rabbit antiserum against the major internal protein, p27, of a psoriasis associated retrovirus-like particle has been applied in an immunofluorescence assay for the detection of antigens cross reacting with p27 in patients with psoriatic arthritis, seronegative rheumatoid arthritis, or ankylosing spondylitis. Antigens reacting with anti-p27 antibodies were present in lymphocytes from blood or synovial fluid from all patients examined. However, the expression was restricted to 0.01-0.1% of the cells. Among the positive p27 cells were cells reacting with markers for T, B, or NK cells. The anti-p27 antibodies also reacted with mononuclear cells in the synovial membrane and with the internal wall of some small or medium sized vessels in sections of synovial biopsy specimens from the patients with chronic arthritis. The reaction with mononuclear synovial membrane cells was restricted to approximately 0.1% of the cells. Blood lymphocytes or synovial sections from healthy persons did not react with the anti-p27 antibodies. The implication of these observations in the pathogenesis of chronic arthritis in man is discussed.
PMCID: PMC1001770  PMID: 3904644
2.  Lymphocytes transformed by Epstein-Barr virus. Induction of nuclear antigen reactive with antibody in rheumatoid arthritis 
The Journal of Experimental Medicine  1978;147(4):1018-1027.
Sera from approximately two-thirds of patients with rheumatoid arthritis contain an antibody which is reactive with a nuclear antigen present in human B-lymphocyte tissue culture cells. The immunological reaction can be demonstrated by precipitation and immunofluorescence. Evidence is present that the reactive nuclear antigen is associated with Epstein-Barr (EB) virus-transformed lymphocytes. Normal human peripheral blood lymphocytes did not contain the nuclear antigen reactive with rheumatoid arthritis sera, but after infection with EB virus, they showed increasing amounts of reactive nuclear antigen as the cells were transformed into continuous lines. Several established human and simian lymphocyte cell lines known to carry EB viral genomes were shown to contain rheumatoid arthritis-associated nuclear antigen. Evidence is presented which suggests that the rheumatoid arthritis- associated nuclear antigen is different from the previously described EB nuclear antigen.
PMCID: PMC2184239  PMID: 206643
3.  Immunisation of guinea-pigs with circulating immune complexes from patients with rheumatoid arthritis. 
Annals of the Rheumatic Diseases  1984;43(5):749-754.
Sixteen guinea-pigs were immunised with immune complexes isolated from serum of nine patients with rheumatoid arthritis. The resulting antisera were analysed by radioimmunoassays. All guinea-pig sera were extensively absorbed with normal human serum. After this absorption eight guinea-pig sera contained antibodies specific for immune complexes isolated from the sera of three patients. One of these antisera reacted not only with immune complexes (and serum) from the corresponding patient but also with immune complexes (and sera) from other patients with rheumatoid arthritis. The antigen(s) to which the guinea-pig antibodies were directed sedimented as IgM, and they bound to IgG Sepharose. Therefore the guinea-pig sera were absorbed with IgM-rheumatoid factors isolated from the serum of the corresponding patient. After this absorption, the guinea-pig sera had lost their reactivity with immune complexes. We conclude that these antisera did not detect an exogenous antigen in immune complexes from patients with rheumatoid arthritis. The positive reactions found were due to antibodies specific for (idiotypic?) antigenic determinants on IgM-rheumatoid factors.
PMCID: PMC1001521  PMID: 6208856
4.  Antibody-mediated leucocyte cytotoxicity to Chang human liver cells in rheumatoid arthritis and other diseases. 
The incidence of an IgG-antibody which induces lymphocyte cytotoxicity to Chang human liver cells in culture was estimated in the sera of patients with rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, psoriatic arthritis, Crohn's disease, ulcerative colitis, and in healthy controls. It was found in 4.1% of control subjects and in 31% of patients with rheumatoid arthritis. None of the other patient groups differed from the control group. This may be the first demonstration of an antibody response to an antigen or antigens which is almost entirely confined to patients with rheumatoid arthritis. The possibility that an antigenic similarity exists between the rheumatoid synovial membrane and Chang cells is currently under investigation.
PMCID: PMC1006502  PMID: 1275578
5.  Antibody to the Rheumatoid Arthritis Nuclear Antigen 
Journal of Clinical Investigation  1980;65(5):1238-1242.
Most patients with seropositive rheumatoid arthritis, and a variable but lesser percentage of normal subjects, have precipitating antibodies to a nuclear antigen, rheumatoid arthritis nuclear antigen, present in Epstein-Barr virus-infected human B lymphoblastoid cells. We have used a sensitive indirect immunofluorescence assay for antibody to rheumatoid arthritis nuclear antigen in a study of patients with infectious mononucleosis and healthy control subjects. Of 110 sera from normal, college-age cadets, 58 were from individuals without prior Epstein-Barr virus infection, as indicated by the lack of antibody to viral capsid antigen. All of these also lacked activity to rheumatoid arthritis nuclear antigen. 52 sera were positive for antibody to viral capsid antigen, and antibody to rheumatoid arthritis nuclear antigen was present in 26 (50%) of these. In 67 sequential sera from 11 college-age students with infectious mononucleosis who became positive for antibody to rheumatoid arthritis nuclear antigen, only 2 were positive during the 1 mo. Thereafter the incidence and titers increased progressively through the 1st yr after infection. This time-course resembled that for the development of antibody to Epstein-Barr nuclear antigen, another transformation antigen in Epstein-Barr virus-infected B lymphocytes. The development of positivity for both was much later than that of antibody to the structural viral capsid antigen, which in the current study was always positive by 1 wk. Thus, antibody to rheumatoid arthritis nuclear antigen is present in a large proportion of normal individuals and can now be clearly ascribed, from both in vivo and in vitro studies, to prior infection with Epstein-Barr virus.
PMCID: PMC371458  PMID: 6245108
6.  Polymerase chain reaction fails to incriminate exogenous retroviruses HTLV-I and HIV-1 in rheumatological diseases although a minority of sera cross react with retroviral antigens. 
Annals of the Rheumatic Diseases  1994;53(11):749-754.
OBJECTIVES--To investigate the presence of antibodies to HTLV and HIV retroviral antigens in the rheumatological diseases rheumatoid arthritis (RA), polymyositis/dermatomyositis (PM/DM), primary Sjögren's syndrome (pSS), and systemic lupus erythematosus (SLE), and to use polymerase chain reaction (PCR) to seek these exogenous retroviruses in proviral form in cellular DNA from these patients. METHODS--Thirty patients with active RA, 13 with PM, 14 with pSS and five with SLE were recruited and their sera tested for antibodies to HTLV-I in enzyme linked immunosorbent assay (ELISA) and Western blot analysis. Seropositivity to HIV-1 was also sought. DNA was extracted from peripheral blood lymphocytes, synovial tissue and muscle biopsies and tested by polymerase chain reaction using consensus primers for HTLV-I and HIV-1. RESULTS--In HTLV-I ELISA, nine rheumatological sera (4/30 RA, 3/13 PM/DM and 2/5 SLE patients) were considered positive; 14 from pSS patients and 30 from normal subjects were negative. In a control group which included osteoarthritis, Crohn's disease and bacterial endocarditis patients, only two of 80 proved positive in this system. Validation of these sera by Western blotting generally revealed weak reactivity against a variety of HTLV-I antigens. PCR of genomic DNA derived from patients' peripheral blood mononuclear cells did not reveal the presence of HTLV-I and HIV-1 target sequences. CONCLUSIONS--This study shows that PCR precludes HTLV-I and HIV-1 infection as causative agents in these rheumatological diseases although a minority of patients possess antibodies that are weakly cross-reactive with retroviral antigens.
PMCID: PMC1005456  PMID: 7826136
7.  Search for viral nucleic sequences in rheumatoid cells. 
Annals of the Rheumatic Diseases  1979;38(5):456-462.
DNA and RNA were extracted from synovial membranes, synovial fibroblast cells, peripheral blood lymphocytes, and synovial fibroblast cells strains derived from patients with rheumatoid arthritis and other joint conditions. They were hybridised after immobilisation on nitrocellulose filters with iodinated viral nucleic acids extracted from measles, rubella virus, SV--40, and a retrovirus, RD--114. In addition, in situ-hybridisation was carried out on sections of synovial membranes by means of iodinated measles and rubella virus RNA. In no case did any hybridisation occur. Positive control systems included synovial fibroblast strains transformed with SV--40, LLC--MK2 cells chronically infected with rubella virus and RD cells infected with RD--114. It was concluded tht the synovial cells did not contain viral genomes of measles, rubella virus, SV--40, or RD--114, or at least at a level equivalent to the positive control cells.
PMCID: PMC1000392  PMID: 229779
Rheumatoid factors in the sera of patients with rheumatoid arthritis appear to be specifically directed against genetically determined "antigens" in human γ-globulin. At least eight rheumatoid factors of differing specificity exist; usually several are present in combination in the same serum. The different rheumatoid factors can be readily detected through their pattern of reactivity with anti-Rh antibodies from different individuals. Rheumatoid factors in diseases other than rheumatoid arthritis were found to have a more restricted specificity, contrasted to the broader reactivity of the factors in most rheumatoid arthritis sera. A specificity similar to that for incomplete antibodies was not demonstrated for the reaction of rheumatoid factors with aggregated γ-globulin or with γ-globulin to form the "22S complex." In certain instances, using the anti-Rh system, rheumatoid factors were found to react poorly with the patient's own γ-globulin, compared to that of other individuals of different genetic γ-globulin types. These results, as well as additional indirect evidence, indicate that the rheumatoid factors can possess isospecificity. However, a certain degree of autospecificity was also found which was most clearly evident through complex formation with the patients own γ-globulin and in the reaction with aggregates. The relevance of these findings to possible isoantibody as well as autoantibody concepts is discussed.
PMCID: PMC2137453  PMID: 13702406
9.  Antikeratin antibodies in serum and synovial fluid show specificity for rheumatoid arthritis in a study of connective tissue diseases. 
Annals of the Rheumatic Diseases  1985;44(7):450-454.
Tests for antikeratin antibodies (AKA) were performed on 2152 disease-associated and control sera by indirect immunofluorescence (IF) on rat oesophagus substrate. The incidence of AKA was significantly raised in rheumatoid arthritis (37%) in comparison with systemic sclerosis (8%), psoriasis (7%), ankylosing spondylitis (6%), systemic lupus erythematosus (3%), and normal controls (2%). AKA were detected in synovial fluid obtained from patients with rheumatoid arthritis (RA) (48%) but not from patients with other conditions. Further experiments on AKA-positive sera showed reactivity with stratum corneum of rabbit prepuce and lips. A specific rabbit antihuman keratin antiserum was shown, by IF and inhibition studies, to have a different specificity from that of spontaneous human AKA. AKA were associated with the presence of subcutaneous nodules in RA (p = 0.05), but not with Raynaud's phenomenon, Sjögren's syndrome, or HLA-DR4 positivity. Rheumatoid factor (RF) was not associated with AKA either in RA or in RF-positive disease controls.
PMCID: PMC1001675  PMID: 2411231
10.  Rubella virus and rheumatoid arthritis. 
A collection of synovial fibroblasts from 19 patients with rheumatoid arthritis (RA) and 12 patients with osteoarthrosis or other non-RA disease has been examined for rubella virus antigens by immunofluorescence and radioimmunoassay with negative results. Eluates of synovial membrane prepared under conditions likely to dissociate antigen-antibody complexes have shown no rubella antibody. A serological survey of RA patients and those with other forms of arthritis has shown no differences in the frequency or levels of rubella haemagglutination-inhibiting antibody. These results provide little support for various hypotheses that a persistent infection with rubella virus underlies or initiates the rheumatoid process.
PMCID: PMC1006622  PMID: 320944
11.  Lack of Detection of Human Retrovirus-5 Proviral DNA in Synovial Tissue and Blood Specimens From Individuals With Rheumatoid Arthritis or Osteoarthritis 
Arthritis and rheumatism  2006;55(1):123-125.
Prior studies have suggested an association of human retrovirus 5 with rheumatoid arthritis. The purpose of this study was to determine if human retrovirus-5 proviral DNA is present in synovial tissue and blood specimens from patients with rheumatoid arthritis or osteoarthritis, or those without joint disease.
Synovial tissue and whole blood from 75 patients with rheumatoid arthritis, 75 patients with osteoarthritis, and 50 patients without a primary arthritis diagnosis were assayed by real-time quantitative polymerase chain reaction (PCR) using primers that amplify a 186-bp fragment of human retrovirus-5 proviral DNA.
A total of 200 tissue specimens, 200 mononuclear cells, and 196 of 200 granulocyte specimens tested negative for human retrovirus-5 proviral DNA. No association between human retrovirus 5 and rheumatoid arthritis or osteoarthritis (P = 0.516) was identified. Granulocyte specimens from 4 patients, 2 with rheumatoid arthritis and 2 with osteoarthritis, yielded a low positive human retrovirus-5 proviral DNA signal (83–1,365 copies of human retrovirus-5 proviral DNA/ml blood).
Contrary to prior reports, we did not find an association between human retrovirus 5 and rheumatoid arthritis or osteoarthritis using a real-time PCR assay. Our findings are consistent with the recent finding that human retrovirus 5 is actually rabbit endogenous retrovirus H.
PMCID: PMC1464419  PMID: 16463423
Human retrovirus-5; Rheumatoid arthritis; Osteoarthritis
12.  Arthritis in a human T lymphotropic virus type I (HTLV-I) carrier. 
Annals of the Rheumatic Diseases  1990;49(9):718-721.
The case is described of a 57 year old woman with polyarthritis fulfilling the 1987 revised criteria of the American Rheumatism Association for rheumatoid arthritis, accompanied by clinical carrier state infection of HTLV-I. Anti-HTLV-I IgM antibodies were detected by western blot analysis in her synovial fluid and serum. Atypical lymphocytes with nuclear convolutions were found in synovial fluid and synovial tissue obtained from the affected knee joint, suggesting in situ activation of HTLV-I infected lymphocytes in the affected synovial compartment. The HTLV-I antigens were detected (1.2%) in short term cultured synovial fluid lymphocytes, by indirect immunofluorescence. These findings supported the possibility that HTLV-I has a role in triggering or modifying inflammation in the synovial compartment.
PMCID: PMC1004211  PMID: 2241290
13.  The gut as an inductive site for synovial and extra-articular immune responses in rheumatoid arthritis. 
Annals of the Rheumatic Diseases  1994;53(6):377-382.
OBJECTIVES--To analyse the immunological interactions between the gut lymphoid tissue, synovium, and peripheral blood compartments in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). METHODS--Patients with RA and AS and healthy controls were orally or parenterally immunised with an influenza virus vaccine. Antigen-specific antibody responses were measured at the single cell level by ELISPOT assay using lymphocytes isolated from peripheral blood and from enzymatically dispersed synovial tissues. RESULTS--Both oral and parenteral immunisations induced antigen-specific antibody-secreting cells in the synovial tissue of patients with RA. Parenterally immunised patients with RA showed significantly decreased antigen-specific antibody responses in peripheral blood compared with patients with AS and with healthy controls. In contrast, oral vaccination evoked comparable peripheral blood antibody responses in all three study groups. CONCLUSIONS--Despite a decreased immune responsiveness in the systemic compartment, the functional status of the gut-associated lymphoid tissue in patients with RA is intact. In addition, there is evidence that the lymphocytes in the inflamed joints are accessible for signals both from the systemic and mucosal compartments. The findings of immunological 'cross-talk' are relevant to future vaccination and tolerization procedures in patients with RA.
PMCID: PMC1005352  PMID: 8037496
14.  Antibody-dependent cell-mediated cytotoxicity in selected autoimmune diseases. 
Journal of Clinical Investigation  1976;58(1):173-179.
Antibody-dependent cell-mediated cytotoxicity mediated by peripheral blood lymphocytes was studied in patients with systemic lupus erythematosus, polyarteritis nodosa. Sjogren's syndrome, and rheumatoid arthritis. The target cells were chicken erythrocytes coated with rabbit anti-chicken erythrocyte antibody. Antibody-dependent cell-mediated cytotoxic activity was normal in Sjogren's syndrome and rheumatoid arthritis but significantly decreased (P is less than 0.001) in active systemic lupus erythematosus and in two patients with polyarteritis nodosa. A partial regeneration of antibody-dependent cell-mediated cytotoxic activity was obtained by treatment with pronase and DNase followed by overnight incubation. Sera from patients with systemic lupus erythematosus inhibited antibody-dependent cell-mediated cytotoxic activity of normal lymphocytes. The inhibitory activity was studied by specific immunoadsorption and sucrose density geadient ultracentrifugation. Removal of IgG but not IgM greatly reduced inhibition. Inhibitory factors were present in 7S and heavier fractions containing IgG. Five systemic lupus erythematosus patients were studied serially to determine if improvement in clinical status could be correlated with a decrease in serum inhibitory factors as studied by inhibition of normal antibody-dependent cell-mediated cytotoxicity. Indeed, a greater serum inhibitory capacity was found in each patient during periods of greater disease activity.
PMCID: PMC333168  PMID: 6490
15.  Serum Reactivity against Borrelia burgdorferi OspA in Patients with Rheumatoid Arthritis▿  
Clinical and Vaccine Immunology : CVI  2007;14(11):1437-1441.
Lyme arthritis and rheumatoid arthritis share common clinical features and synovial histology. It is unclear whether they also share similar pathogenesis. Previous studies have shown that the severity and duration of Lyme arthritis correlate directly with serum concentrations of antibody against outer surface protein A (OspA) of the causative pathogen Borrelia burgdorferi. We tested the sera of 68 subjects with rheumatoid arthritis, 147 subjects with other autoimmune diseases, and 44 healthy subjects who had never had Lyme disease, as well as sera of 16 patients who had Lyme disease, for reactivity against the B. burgdorferi OspA protein. The sera of about a quarter of the rheumatoid arthritis patients and a 10th of the autoimmune disease and Lyme disease patients reacted against OspA antigen. Of 50 rheumatoid arthritis patients who could be evaluated for disease severity, a 28-joint count disease activity score of >2.6 was noted for 11 of 15 (73%) patients whose sera reacted against OspA antigen and 13 of 35 (37%; P < 0.05) whose sera were nonreactive. Serum reactivity against OspA antigen is associated with the pathogenesis of rheumatoid arthritis.
PMCID: PMC2168181  PMID: 17881508
16.  Reaction of antibodies to rheumatoid arthritis nuclear antigen with a synthetic peptide corresponding to part of Epstein-Barr nuclear antigen 1. 
Annals of the Rheumatic Diseases  1988;47(4):270-279.
Antibodies to rheumatoid arthritis nuclear antigen (RANA) are detected by immunodiffusion (ID) and immunofluorescence (IF), though reports of the identity of the antigen(s) have been conflicting. In this study it is shown conclusively that ID and IF anti-RANA react with epitopes on Epstein-Barr nuclear antigen 1 (EBNA-1) and that the major epitope detected by immunofluorescence is represented by a synthetic peptide, P62, corresponding to part of EBNA-1. In an enzyme linked immunosorbent assay (ELISA) anti-P62 antibodies in 35 rheumatoid arthritis sera were threefold higher than those of 35 age and sex matched controls, with the highest levels occurring in young patients with active joint disease.
PMCID: PMC1003506  PMID: 2452607
17.  Activation pathways of synovial T lymphocytes. Expression and function of the UM4D4/CDw60 antigen. 
Journal of Clinical Investigation  1990;86(4):1124-1136.
Accumulating evidence implicates a central role for synovial T cells in the pathogenesis of rheumatoid arthritis, but the activation pathways that drive proliferation and effector function of these cells are not known. We have recently generated a novel monoclonal antibody against a rheumatoid synovial T cell line that recognizes an antigen termed UM4D4 (CDw60). This antigen is expressed on a minority of peripheral blood T cells, and represents the surface component of a distinct pathway of human T cell activation. The current studies were performed to examine the expression and function of UM4D4 on T cells obtained from synovial fluid and synovial membranes of patients with rheumatoid arthritis and other forms of inflammatory joint disease. The UM4D4 antigen is expressed at high surface density on about three-fourths of synovial fluid T cells and on a small subset of synovial fluid natural killer cells; in synovial tissue it is present on more than 90% of T cells in lymphoid aggregates, and on approximately 50% of T cells in stromal infiltrates In addition, UM4D4 is expressed in synovial tissue on a previously undescribed population of HLA-DR/DP-negative non-T cells with a dendritic morphology. Anti-UM4D4 was co-mitogenic for both RA and non-RA synovial fluid mononuclear cells, and induced IL-2 receptor expression. The UM4D4/CDw60 antigen may represent a functional activation pathway for synovial compartment T cells, which could play an important role in the pathogenesis of inflammatory arthritis.
PMCID: PMC296841  PMID: 2212003
18.  Detection of Anti-Glomercular Basement Membrane Antibodies by a Radioimmunological Technique CLINICAL APPLICATION IN HUMAN NEPHROPATHIES 
Journal of Clinical Investigation  1974;54(1):128-137.
A radioimmunoassay for detection of anti-glomerular basement membrane (GBM) antibody was set up with a 70,000 mol wt GBM antigen, labeled with Iodine-125I and containing both types of oligosaccharidic chains present in the whole membrane.
Separation of free radioactive antigens from antigens bound to immunoglobulins was obtained by precipitation with polyethylene glycol (mol wt, 6,000), at a final concentration of 20%. In the presence of normal human or rabbit sera, less than 20% of labeled antigens were precipitated. In the presence of rabbit anti-human GBM antibodies, up to 82% of GBM antigens were precipitated, while in the presence of sera or of kidney eluate from a patient with Goodpasture's syndrome, the precipitation of GBM antigens reached 43%. The avidity of rabbit anti-GBM antibodies for human GBM antigens is higher than that of human anti-GBM antibodies. In the case of Goodpasture's syndrome, the binding of anti-GBM antibodies to labeled antigens was inhibited more efficiently by the disaccharide-containing glycopeptide than by the heteropolysaccharide-containing glycopeptide purified from whole GBM.
Anti-GBM antibodies were searched for in the serum of 300 normal blood donors, of 120 patients with glomerulonephritis (GN) and granular deposits, and of 14 patients with GN and linear deposits of immunoglobulins. After correction for the “nonspecific” precipitation, the average percentage (±1 SD) of labeled antigens precipitated in the serum of normal blood donors was 0.3±3.2%; 12 patients with GN and linear deposits exhibited high circulating anti-GBM antibody titers, while 8% of the patients with GN and granular deposits presented significant, albeit lower, anti-GBM activity in their sera.
PMCID: PMC301532  PMID: 4857905
19.  Detection of p53 in inflammatory tissue and lymphocytes using immunohistology and flow cytometry: a critical comment. 
Journal of Clinical Pathology  1997;50(8):654-660.
AIMS: To analyse the expression of p53 in lymphatic cells found in inflammatory tissues and the peripheral blood by immunological methods. METHODS: Immunohistological analysis of synovial tissues from patients with rheumatoid arthritis and flow cytometric analysis of peripheral blood lymphocytes were performed with anti-p53 antibodies from different sources. RESULTS: The anti-p53 antibodies PAb240, PAb421, and PAb1801 from one supplier bound to the cytoplasm of lymphocytes, fibroblasts, and endothelial cells in rheumatoid synovial tissue, while the same anti-p53 antibodies from other sources and the p53 specific antibodies PAb1620 and DO1 were negative. Using flow cytometry, the antibodies that labelled cells in inflammatory tissues were shown to bind also to peripheral lymphocytes, while the antibodies that were negative in immunohistology did not react with peripheral blood lymphocytes. p53 expression could be confirmed by western blot in rheumatoid synovial tissue, but not in peripheral blood lymphocytes using PAb421 and PAb240 antibodies from our own laboratory, which had been negative in immunohistology. CONCLUSIONS: Demonstration of p53 by western blot is more sensitive and reliable than immunohistology and flow cytometry. Western blot is the gold standard for the demonstration of p53 expression and should be used, whenever possible, to confirm p53 expression in normal tissue shown by immunohistology or flow cytometry. All other reports on p53 expression, especially those obtained using antibodies with an unusual staining pattern must be interpreted with caution.
PMCID: PMC500108  PMID: 9301548
20.  Antibody to intermediate filaments of the cytoskeleton. 
IgM antibodies against cultures of intermediate filaments (IMF) of the cytoskeleton were demonstrated by immunofluorescence in the sera of 94 (80%) of 118 patients with seropositive rheumatoid arthritis. These antibodies reacted with IMF in cultures of both human fetal fibroblasts and laryngeal carcinoma (HEp2) cells. Of 10 patients from whom paired synovial fluids were also available 8 had anti-IMF antibodies in both serum and fluid. In seronegative RA the incidence of anti-IMF was 40%, in ankylosing spondylitis 25%, in osteoarthrosis 16%, and in normal subjects 14%. Only a minority of RA sera positive for anti-IMF antibodies were also positive for smooth muscle antibody. Absorption experiments suggest that in RA anti-IMF is directed at the intermediate filament protein, vimentin.
PMCID: PMC1000867  PMID: 7039524
21.  Humoral immune response against minor collagens type IX and XI in patients with cartilage graft resorption after reconstructive surgery. 
Annals of the Rheumatic Diseases  1994;53(4):229-234.
OBJECTIVES--The humoral immune response against a broad spectrum of cartilage antigens (cellular and matrix antigens) was studied in a group of patients who showed resorption and/or rejection of transplanted cartilage in nasal surgery. METHODS--Sera were obtained from patients with successful and unsuccessful cartilage grafting in the nose, from age and sex-matched healthy donors and from patients with rheumatoid arthritis. Antibodies to cartilage components were analysed by the following methods: (1) indirect immunofluorescence on cartilage sections, (2) ELISA using cultured human chondrocytes, isolated chondrocyte membranes and purified collagens type I, II, III, VI, IX and XI, and (3) immunoblotting with purified collagens and chondrocyte cell membranes. RESULTS--In the cartilage grafting group showing resorption problems, levels of anti-collagen antibodies were significantly higher against native collagen types IX (p < 0.002) and XI (p < 0.002) compared with the non-resorption group and the normal donors. Both transplantation groups revealed elevated reactivities against isolated chondrocytes in the ELISA. In contrast, no reactivity was detectable against collagens type II, III, and VI and chondrocyte cell membranes by both ELISA and immunoblotting. CONCLUSIONS--These data demonstrate for the first time the existence of a humoral immune response, primarily directed against the so called 'minor cartilage collagens', in patients showing cartilage resorption. Autoreactivities to collagen which are typical of inflammatory rheumatic diseases may also play an important role in the repeated failure of cartilage grafting.
PMCID: PMC1005300  PMID: 8203950
22.  Viruses and lymphocytes in rheumatoid arthritis. I. Studies on cultured rheumatoid lymphocytes. 
Annals of the Rheumatic Diseases  1979;38(6):507-513.
Synovial fluid lymphocytes from patients with rheumatoid arthritis have been examined for evidence of a productive infection with retroviruses by electron microscopy, labelling with 3H-uredine, growth in soft agar, and culturing in conditioned medium. No such viruses were detected. In addition, the synovial lymphocytes were activated before fusion and cocultivation with several cell lines which have proved permissive for primate retroviruses. Monitoring these cultures subsequently by reverse transcriptase assay, labelling with 3H-uridine, and membrane immunofluorescence gave no indication that retroviruses were present.
PMCID: PMC1000410  PMID: 539843
23.  Anti-cartilage antibody. 
Journal of Clinical Pathology  1979;32(8):826-831.
Antibody to cartilage has been demonstrated by indirect immunofluorescence on rat trachea in the serum of about 3% of 1126 patients with rheumatoid arthritis. Titres ranged from 1:20 to 1:640. The antibody was not found in 284 patients with primary or secondary osteoarthritis or in 1825 blood donors, nor, with the exception of two weak reactors, in 1314 paraplegic patients. In most cases the antibody appears to be specific for native type II collagen. Using this as an antigen in a haemagglutination test 94% of anti-cartilage sera were positive, whereas among 100 rheumatoid control sera there were only three weak positives. More than 80% of patients with antibody had some erosion of articular cartilage, but there was no correlation with age, sex, duration of disease, nor any recognisable clinical event or change.
PMCID: PMC1145817  PMID: 389957
24.  Novel 68 kDa autoantigen detected by rheumatoid arthritis specific antibodies. 
Annals of the Rheumatic Diseases  1995;54(5):355-360.
OBJECTIVE--To improve the understanding of the pathogenesis of rheumatoid arthritis (RA) by identifying novel, disease specific autoantibodies. METHODS--Total protein preparations from synovial membranes were separated electrophoretically and immunoblotted. Sera from RA patients were screened for predominant immunoreactions by blotting. A 68 kDa antigen target of the most predominant reaction was detected and further characterised. RESULTS--The dominant immunoreaction in most of the RA sera tested was with a 68 kDa antigen. The antigen is probably ubiquitously expressed. It has an isoelectric point of 5.1, is O-glycosylated, and is located in the endoplasmic reticulum, the cytoplasm, or both. Antibodies to the 68 kDa autoantigen were present in 64% of 167 RA patients tested, and could also be detected in seronegative RA patients, but were present in only 1% of 98 patients with other rheumatic diseases. They could not be detected in 55 healthy controls. CONCLUSIONS--Because of its high sensitivity (64%) and specificity (99%), the anti-68 kDa autoantibody not only provides another valuable parameter for diagnosis, but also represents an antibody that may be involved in the pathological mechanisms leading to RA. This hypothesis can be tested by investigating if 68 kDa specific T cells are present in RA patients.
PMCID: PMC1005594  PMID: 7794040
25.  Interaction in vitro between synovial cells and autologous lymphocytes and sera from arthritis patients. 
Journal of Clinical Pathology  1975;28(7):550-558.
Synovial cells from patients with rheumatoid arthritis (RA) when grown in vitro in media supplemented with 20% fetal calf serum failed to show any difference in growth rate, life span, uptake of tritiated thymidine or cellular and nuclear characteristics when compared with synovial cells from patients with osteoarthritis or other joint diseases grown similarly in 20% serum enriched medium. There was also no evidence that lymphocytes and/or sera from RA patients were more cytotoxic to autologous synovial cells than sera and/or lymphocytes from OA patients. It is unlikely that antisynovial antibodies or lymphocytes from RA patients act as triggers for synovial damage.
PMCID: PMC475770  PMID: 1097473

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