bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential reactivity of rheumatoid synovial cells and serum rheumatoid factors to human immunoglobulin g subclasses 1 and 3 and their CH3 domains in rheumatoid arthritis
Authors: Robbins Dick L. , Benisek William F. , Benjamini Eliezer , Wistar Richard 
Published: February 2007

Abstract19S IgM rheumatoid factors (RF) are polyclonal autoantibodies that may play an important pathogenic role in sustaining inflammatory synovitis in rheumatoid arthritis (RA). RF in RA have reactivity for as‐yet‐uncharacterized antigenic determinants in IgG Fc. We hypothesized that qualitative differences might exist between some of these RF molecules, and that differences such as reactivity and affinity might characterize more pathogenic RF molecules. Previous observations in our laboratory indicate that RF produced by rheumatoid synovial cells (RSC) have greater reactivity with human IgG and IgG3 subclass, in contrast to serum RF, which has greater reactivity with rabbit IgG and human IgG1. These observations were made using a complement‐dependent RF plaque‐forming cell assay. The purpose of this study was to validate and extend those observations. Therefore, we examined the reactivity of RSC and serum RF with human and rabbit IgG and the reactivity and avidity of RSC‐RF for IgG1 and IgG3 molecules and Fab, F(ab')2, and pFc' fragments thereof in a solid‐phase enzyme immunoassay. In particular, we found: 1) RSC‐RF had at least twice as much reactivity with human IgG as with rabbit IgG; 2) serum RF had approximately equal reactivity with human and rabbit IgG; 3) RSC‐RF had greater reactivity and avidity for IgG3 and IgG3 pFc' than for IgG1; and 4) RSC‐RF was nonreactive with Fab or F(ab')2 from either IgG1 or IgG3. These results suggest that the major antigenic determinant for RSC‐RF resides in the CH3 domain of the IgG3 molecule. Precise characterization of this epitope may provide further insight into the etiology and pathogenesis of RA.
Monocyte fc receptor function in rheumatoid arthritis. enhanced cell‐binding of igg induced by rheumatoid factors
Authors: Mackinnon Susan K. , Starkebaum Gordon 
Published: February 2007

AbstractMonocytes from 11 patients with rheumatoid arthritis and 10 control subjects were purified by countercurrent elutriation. Rheumatoid arthritis monocytes had more cell‐associated IgG (P < 0.001) and bound more 125I‐labeled heat‐aggregated IgG in vitro (P < 0.02) than did monocytes from control subjects. Interaction of rheumatoid factor (RF) with monocytes was then investigated. Purified 125I‐labeled IgM‐RF and IgG‐RF bound directly to monocytes from normal individuals. Furthermore, preincubation of normal monocytes with RF augmented subsequent binding of aggregated IgG to the cells. We conclude that monocyte‐associated RF can enhance binding of IgG‐containing immune complexes to the cells and can exaggerate the measured number of Fc receptors. Such cell‐bound RF may affect clearance of immune complexes by the reticuloendothelial system in vivo.
The work dynamics of the person with rheumatoid arthritis
Authors: Yelin Edward , Henke Curtis , Epstein Wallace 
Published: February 2007

AbstractThis paper traces the work history of patients with rheumatoid arthritis (RA) from the year of diagnosis to 1985. The paper also describes the risk factors for work loss among patients with RA. It uses data from a panel of 698 RA patients, observed for 4 years, from the practices of a random sample of northern California rheumatologists. Of these 698, 353 had worked for pay at some point in their lives. Three hundred six of the 353 had worked when diagnosed as having RA. Of these 306, 157 (51%) were no longer working in 1985. Forty‐seven individuals started working after the onset of illness, but of these, approximately one‐third had stopped working by 1985. In all, 50% of RA patients with some work experience stopped working within a decade of diagnosis, 60% within 15 years, and 90% within 30 years. We found that the probability of work loss is lessened among persons in jobs that have few physical requirements, among those with high levels of discretion over the pace and activities of work, and among those who were able to stay on the job held when the diagnosis was made. The probability of work loss is increased among service workers. The findings of this longitudinal study, showing that work characteristics profoundly alter the probability of work loss among persons with RA, are consistent with the findings of our earlier cross‐sectional studies of work outcome and RA.
Viral and host genetic factors influence encephalomyocarditis virus—induced polymyositis in adult mice
Authors: Miller Frederick W. , Love Lori A. , Biswas Tapas , McClintock Patrick R. , Notkins Abner Louis , Plotz Paul H. 
Published: February 2007

AbstractRecent research findings implicate picornaviruses in the etiology of human polymyositis/dermatomyositis and suggest that genetic factors play a role in susceptibility to these diseases. We compared 2 variants of encephalomyocarditis (EMC) virus for their ability to induce polymyositis in adult mice, and evaluated what role the genetic background of the host plays in the degree of myositis induced. While BALB/c mice developed minimal myositis when infected with a diabetogenic variant (EMC‐D), the same strain inoculated with a newly isolated myopathic variant (EMC‐221A) developed viral dose—dependent elevations in muscle‐associated enzymes, bilateral limb muscle weakness, and the histopathologic changes of severe polymyositis. Mice with different genetic backgrounds showed significantly different susceptibilities to EMC‐221A. These data suggest that the severity of polymyositis induced by EMC virus is influenced by both the viral and host genomes.
Activation of complement and coagulation in juvenile dermatomyositis
Authors: Scott John Paul , Arroyave Carlos 
Published: February 2007

AbstractIn patients with juvenile dermatomyositis (JDM), small vessel occlusion and thrombosis result in a decrease in the capillary: muscle fiber ratio. We studied 15 patients with JDM. Six of 7 patients with clinically active JDM had elevated levels of C3d. Moreover, concentrations of fibrinopeptide A and factor VIII‐related antigen were significantly increased in patients with clinically active JDM.
Atlantoaxial (C1‐C2) facet joint osteoarthritis: a distinctive clinical syndrome
Authors: Halla James T. , Hardin Joe G. 
Published: February 2007

AbstractOsteoarthritis of the atlantoaxial facet joints was identified radiologically in 27 patients, and these comprised 4% of all outpatients with osteoarthritis or degenerative disease of the spine seen during a 36‐month period. These patients had a clinical syndrome which differed from those seen in patients who have subaxial degenerative disease of the spine or myofascial cervical pain. Occipital pain, occipital trigger points, crepitus in the occipital region, and a rotational head tilt deformity (in 13 patients, usually associated with collapse of 1 of the lateral masses [facets]), were the major features of this distinctive syndrome.
Is anticardiolipin activity a cross‐reaction of anti‐DNA or a separate entity?
Authors: Smeenk Ruud J. T. , Lucassen Wim A. M. , Swaak Tom J. G. 
Published: February 2007

AbstractPutative cross‐reactions between anti‐DNA and anticardiolipin activities were studied using sera of different patients and a panel of monoclonal antibodies to DNA. Sera were obtained from patients with systemic lupus erythematosus, from patients with syphilis, and from heroin addicts who showed a biologic false‐positive result on the serologic test for syphilis. While the patients with syphilis and the heroin addicts had elevated levels of anticardiolipin antibodies in their circulation, no reactivity with DNA was observed in these sera. Sera from systemic lupus erythematosus patients often showed both anti‐DNA and anticardiolipin activity. Although a correlation between anti‐DNA and anticardiolipin titers was found, this did not always result from cross‐reactivity of the same population of antibodies. In fact, we observed a relationship between cross‐reactivity and antibody avidity. Anti‐DNA of high avidity to DNA showed little cross‐reactivity with cardiolipin. Anticardiolipin activity in such sera was based on the presence of specific anticardiolipin antibodies. Anti‐DNA of low avidity was found to cross‐react with cardiolipin. Among monoclonal antibodies to DNA, we found that cross‐reactions with cardiolipin were rare: only 6 of 55 anti‐DNA clones produced antibodies that also reacted with cardiolipin.
D‐penicillamine therapy and interstitial lung disease in scleroderma. a long‐term followup study
Authors: Clerck Luc S. De , Dequeker Jan , Francx Luc , Demedts Maurits 
Published: February 2007

AbstractSequential lung function tests were performed on 17 scleroderma patients who were treated with D‐penicillamine (DP) (total of 66 treatment years) and on 10 control scleroderma patients who were not treated or were treated with low‐dose prednisone (total of 25 treatment years). Cusum plots showed significant differences between the 2 groups in their cumulative changes in carbon monoxide diffusing capacity (DLco) (P < 0.005) and in DLco/lung volume (P < 0.02). The end value of the DLco was > 10% lower than the initial value in 3 of the 17 DP‐treated patients versus 5 of the 10 control patients (P < 0.01, Fisher's exact probability test); in 3 DP‐treated patients and 8 control patients (P < 0.003, Fisher's exact probability test), the end value of the DLco/lung volume was >10% lower than the initial value. We conclude that DP has a beneficial effect on interstitial lung disease in patients with scleroderma.
T cytotoxic and helper cells are markedly increased, and t suppressor and inducer cells are markedly decreased, in rheumatoid synovial fluids
Authors: Goto Makoto , Miyamoto Terumasa , Nishioka Kusuki , Uchida Shoji 
Published: February 2007

AbstractSynovial fluid lymphocytes and paired peripheral blood lymphocytes from 28 patients with rheumatoid arthritis were analyzed by 2‐dimensional flow cytometry. We found that the composition of the lymphocyte population is different in synovial fluid compared with that in peripheral blood, in that there were increased proportions of Ia+ Leu‐2a+/Leu‐15– (T cytotoxic) cells and Leu‐3a+/Leu‐8– (T helper) cells, together with marked decreases in Leu‐2a+/Leu‐15+ (T suppressor) cells and Leu‐3a+/Leu‐8+ (T inducer) cells. These findings suggest that the unique composition of synovial fluid lymphocytes might be the result of T cell activation by some mechanism that is not known.
HLA–D region epitopes associated with juvenile arthritis. recognition by alloreactive t cell clones and alloantisera
Authors: Myers Linda K. , Ball Edward J. , Nunez Gabriel , Fink Chester W. , Stastny Peter 
Published: February 2007

AbstractThe HLA–D region antigens DR5 (wll, w12), DRw6 (w13,w14), DRw8, DRw52, and DQw1 have previously been shown to be increased in frequency in subsets of patients with juvenile arthritis. Since the HLA–D region is complex (composed of at least 3 subregions encoding multiple molecules, each in turn presenting multiple alloantigenic epitopes), we sought to clarify whether one strongly associated factor might explain the previous findings. To search for the pertinent HLA–D region stimulatory epitopes, alloreactive T cells were primed against DR5 and DRw6 haplotypes and cloned by limiting dilution. Three T cell clones and 1 alloantiserum met the criteria for significant association with juvenile arthritis on patient testing, including DR5, DRw6, and DRw8 haplotypes. Monoclonal antibody blocking revealed that all 4 recognized epitopes on DR subregion products. For 2 of the clones, the relative risks for JA (10.5 and 9.4) were higher than the risks with any other previously described typing reagents.
Deficiency of the suppressor inducer subset of T lymphocytes in rheumatoid arthritis
Authors: Emery Paul , Gentry Kay C. , Mackay Ian R. , Muirden Ken D. , Rowley Merrill 
Published: February 2007

AbstractNew monoclonal antibodies allow CD4 lymphocytes to be categorized into helper/inducer (HI) CD4+ 4B4+, and suppressor inducer (SI) CD4+ 2H4+ subpopulations. Blood and synovial lymphocytes from 30 patients with rheumatoid arthritis (RA), 13 patients with other articular diseases, and 24 control subjects were exposed to these monoclonal antibodies and analyzed by flow cytometry. CD4:CD8 ratios were similar for the 3 groups. In RA patients, there was a depletion of SI cells in blood and synovial fluid, and the ratio of HI cells to SI cells was elevated, particularly in the synovial lymphocytes. These data provide new evidence for T cell dysregulation in the perpetuation of RA.
Peripheral blood and synovial fluid monocyte activation in inflammatory arthritis. i. a cytofluorographic study of monocyte differentiation antigens and class ii antigens and their regulation by γgm‐interferon
Authors: Firestein Gary S. , Zvaifler Nathan J. 
Published: February 2007

AbstractRecent study of the expression of monocyte differentiation antigens (MAg) and HLA–DR on peripheral blood monocytes (PBM) has led to the recognition of resting and activated monocyte phenotypes. The former is identified by the expression of large amounts of MAg (i.e., Mo2 and 63D3) and small amounts of HLA–DR, while the latter is identified by the reverse. We studied the phenotypes of PBM and synovial fluid monocytes (SFM) of patients with chronic inflammatory arthritis and found that PBM were primarily resting and SFM were usually activated. In addition, we measured the degree of modulation of MAg and HLA–DR by γ‐interferon (γ‐IFN). Patient PBM reacted the same as PBM from normal individuals (i.e., MAg decreased and HLA–DR increased after exposure to γ‐IFN). However, in patient SFM, HLA–DR did not increase with exposure to γ‐IFN because expression was already maximal. Interestingly, MAg could still be down‐regulated on γ‐IFN–treated SFM, even when expression began at a very low level (i.e., activated phenotype). This independent regulation of MAg and HLA–DR suggests that macrophage activating factors other than γ‐IFN may be responsible, in part, for the activated phenotypes observed.
Hla–Dr4 and Gm 1;21 haplotypes are associated with pseudolupus induced by venopyronum dragéeaes
Authors: Grosse‐Wilde Hans , Genth Ekkehard , ühl Audrey Grevesm , Vögeler Udo , Zarnowski Hanabela , Mierau Rudolf , Doxiadis Gabriele , Doxiadis Ilias , Maas Dieter 
Published: February 2007

AbstractThe phenotypic frequencies of human major histocompatibility complex class I, II, and III antigens and immunoglobulin allotypes (Gm factors) were determined in 56 patients (55 women, 1 man) who had lupus‐like disease induced by Venopyronum dragées. The findings in these patients were compared with those of a control group. We found a significant increase of HLA‐DR4 (57.1% versus 26.5%, relative risk [RR] 3.7) and a decrease of HLA‐DR3 (3.6% versus 19.1%, RR 0.16) in the patient group. In addition, the haplotype Gm 1;21 (60.7% versus 32.9%, RR 3.2), and the phenotype Gm 1,3;5,21 (46.4% versus 25.8%, RR 2.5) were significantly increased. Both the haplotype Gm 1;21 and the phenotype Gm 1,3;5,21 are associated with HLA–DR4 in pseudolupus patients but not in controls. The coincidence of HLA–DR4 and Gm 1;21 markedly increases the risk of acquiring pseudolupus (RR 6.9). We conclude that the pathogenesis of pseudolupus is influenced by at least 2 independent genetic factors, A similar HLA association has been described in hydralazine‐induced lupus, and this suggests a common pathogenic mechanism.
Association of a 9.2‐kilobase pvu ii class i major histocompatibility complex restriction fragment length polymorphism with ankylosing spondylitis
Authors: McDaniel D. Olga , Acton Ronald T. , Barger Bruce O. , Koopman William J. , Reveille John D. 
Published: February 2007

AbstractWe analyzed DNA restriction fragment length polymorphism (RFLP) in 53 white ankylosing spondylitis (AS) patients and 92 healthy controls, utilizing a full‐length HLA‐B7 complementary DNA probe. A 9.2‐kilobase (kb) Pvu II fragment was found to be significantly increased in frequency in B27 positive AS patients compared with the B27 positive control group (P = 0.00085, relative risk = 7.2). The presence of both B27 and the 9.2‐kb RFLP in an individual conferred a relative risk for AS of 297, compared with a relative risk of 119 in those who had B27 alone. The 9.2‐kb RFLP appears to be a marker for AS which, with HLA–B27, contributes further to susceptibility to the disease. Our findings indicate that this fragment and HLA–B27 segregate independently in familial studies of AS.
The prevalence of knee osteoarthritis in the elderly. the framingham osteoarthritis study
Authors: Felson David T. , Naimark Allan , Anderson Jennifer , Kazis Lewis , Castelli William , Meenan Robert F. 
Published: February 2007

AbstractTo investigate the prevalence of osteoarthritis (OA) of the knee in elderly subjects, we studied the Framingham Heart Study cohort, a population‐based group. During the eighteenth biennial examination, we evaluated the cohort members for OA of the knee by use of medical history, physical examination, and anteroposterior (standing) radiograph of the knees. Radiographs were obtained on 1,424 of the 1,805 subjects (79%). Their ages ranged from 63–94 years (mean 73). Radiographs were read by a radiologist who specializes in bone and joint radiology, and were graded 0–4 according to the scale described by Kellgren and Lawrence. OA was defined as grade 2 changes (definite osteophytes), or higher, in either knee. Radiographic evidence of OA increased with age, from 27% in subjects younger than age 70, to 44% in subjects age 80 or older. There was a slightly higher prevalence of radiographic changes of OA in women than in men (34% versus 31%); however, there was a significantly higher proportion of women with symptomatic disease (11% of all women versus 7% of all men; P = 0.003). The age‐associated increase in OA was almost entirely the result of the marked age‐associated increase in the incidence of OA in the women studied. This study extends current knowledge about OA of the knee to include elderly subjects, and shows that the prevalence of knee OA increases with age throughout the elderly years.
Metabolism of C4 and linkage analysis in a kindred with hereditary incomplete C4 deficiency
Authors: Wisnieski Jeffrey J. , Nathanson Michael H. , Anderson Jeanne E. , Davis Iii Alvin E. , Alper Chester A. , Naff George B. 
Published: February 2007

AbstractWe studied a kindred in which C4 deficiency had been discovered. Unlike families with total absence of C4, in this kindred C4 deficiency was found to be incomplete, autosomal dominant, not caused by null alleles, and not associated with a high incidence of systemic lupus erythematosus. The deficient state was caused by hyposynthesis of C4, not by hypercatabolism. The locus for incomplete C4 deficiency was not closely linked to the major histocompatibility complex. The abnormal autosomal dominant allele is, apparently, rare, and how it causes decreased synthesis of C4 is unknown.
Restricted heterogeneity of polyclonal rheumatoid factors
Authors: Bouvet Jean‐Pierre , Xin Wu Yu , Pillot Jacques 
Published: February 2007

AbstractThe electrophoretic pattern of rheumatoid factor (RF) was investigated in 40 polyclonal sera, by using radiolabeled IgG. Thirty sera specifically bound IgG aggregates, correlating with their RF titer. The binding pattern was monoclonal or oligoclonal. The molecules responsible were classic RF antibodies, as shown by using purified IgM, inhibition experiments, and by the optimal size of aggregates (2,000–4,000 kd). These data show that RF heterogeneity is restricted in polyclonal sera, and this can have a bearing on several mechanisms.
Effects of gold sodium thiomalate on interferon stimulation of C2 synthesis and HLA–DR expression by human monocytes
Authors: Sanders Karen M. , Carlson Patricia L. , Littman Bruce H. 
Published: February 2007

AbstractGamma‐interferon (γ‐IFN) is a T cell–derived lymphokine that has potent macrophage‐activating properties. It increases Fc receptor density, increases the formation and release of reactive oxygen intermediates, increases the synthesis and release of complement cascade proteins, especially C2 and factor B, and increases class II (HLA–DR) antigen expression. These effects may play a role in the potentiation of inflammation in rheumatoid arthritis. We examined the possibility that gold sodium thiomalate (GST), an effective treatment for rheumatoid arthritis, would inhibit γ‐IFN–mediated stimulation of monocyte/macrophages. GST in concentrations attainable in vivo was shown to inhibit both spontaneous and γ‐IFN–stimulated C2 production up to 50%. GST inhibition could be only partially overcome with increasing concentrations of γ‐IFN. In addition, GST inhibited γ‐IFN–stimulated HLA‐DR expression at the highest concentrations tested (20–50 μg/ml). GST alone in low concentrations (0.1–5 μg/ml) was found to increase HLA‐DR antigen expression as quantitated by several methods, including flow cytometry, cell surface enzyme‐linked immunosorbent assay, and Western blotting. This GST‐stimulated increase in HLA‐DR antigen expression paralleled an increased ability of monocytes to present antigen. The mechanism by which low concentrations of GST stimulate HLA‐DR antigen expression is unclear, but was shown by 35S‐methionine cell labeling not to involve increased HLA‐DR protein synthesis.
Lentivirus infection augments concurrent antigen‐induced arthritis
Authors: Banks Keith L. , Jacobs Cindy A. , Michaels Frank H. , Cheevers William P. 
Published: February 2007

AbstractExperimental antigen–induced arthritis was compared in normal goats and goats infected with caprine arthritis‐encephalitis virus. Although acute arthritis was the same in infected and uninfected animals, the disease lasted 16 weeks longer in the caprine arthritis‐encephalitis virus–infected goats. Our findings suggest that the arthritis caused by this virus is due to events other than, or in addition to, the immune reaction to viral antigens.
Analyses of hla linkage in white families with multiple cases of seropositive rheumatoid arthritis
Authors: C. P.Go Rodney , Alarcón Graciela S. , Acton Ronald T. , Koopman William J. , Vittor Virginia J. , Barger Bruce O. 
Published: February 2007

AbstractFamilies with multiple cases of seropositive rheumatoid arthritis (RA), identified through 2 probands with the disease, were analyzed for genetic linkage between an autosomal susceptibility gene for RA and the HLA loci. These analyses were carried out over a wide range of penetrances (0.1–0.4), with prevalence for the disease fixed at 0.01 or 0.04. In some models, a sporadic frequency of 20% was assumed. Close linkage to the HLA loci was ruled out for all models where the gene was autosomal dominant, except for those with low penetrance and with prevalence set at 0.04. The models in which the gene was autosomal recessive produced results similar to those in models where it was autosomal dominant when prevalence was set at 0.01, and close linkage was ruled out, except at very low penetrances. With prevalence set at 0.04, the autosomal recessive gene model produced log odds scores which were all negative (−2.6 to −0.3). Therefore, the evidence in these families does not support close linkage with HLA, even though a significant DR4 RA population association exists. The data suggest that non‐major histocompatibility complex (MHC) genes may contribute to the development of RA and, therefore, disease susceptibility may involve the genetic interaction of one or more MHC genes and non‐MHC genes, in addition to environmental agents.