bluuebunny/crossref_metadata_2025_split huggingface dataset:
CD4+ and CD8+ T cell expansions using selected TCR V and J gene segments at the onset of giant cell arteritis
Authors: Grunewald Johan , Andersson Rune , Rydberg Lennart , Gigliotti Dulceaydee , Schaufelberger Christopher , Hansson Gö Ran K. , Wigzell Hans 
Published: February 2007

AbstractObjective. To investigate T cell receptor (TCR) Vα/Vβ (and in selected cases, Jβ) usage in CD4+ and CD8+ peripheral blood lymphocytes of patients with giant cell arteritis (GCA), before and after treatment, as well as to analyze the HLA types of these patients.Methods. Flow cytometry, with 10 anti‐TCR V‐specific monoclonal antibodies (MAb), was used. To analyze Jβ usage by cell populations expressing certain Vβ, we used the polymerase chain reaction (PCR) technique, with Vβ‐ and Cβ‐specific primers, Southern blotting of PCR products, and subsequent hybridization with radiolabeled Jβ‐specific probes. HLA typing was performed using the microlymphocytotoxicity technique.Results. Seven of the 9 GCA patients had increased anti‐TCR V MAb reactivities (interpreted as T cell expansions), which in many cases, correlated with clinical signs of disease. A strict preference for particular Jβ segments was found in 3 of 3 expanded CD4+ T cell populations.Conclusion. T lymphocytes expressing specific antigen receptors are implicated in the pathogenesis of GCA.
Suppression of experimental antiphospholipid syndrome and systemic lupus erythematosus in mice by anti‐CD4 monoclonal antibodies
Authors: Tomer Y. , Blank M. , Shoenfeld Yehuda 
Published: February 2007

AbstractObjective. To investigate whether anti‐CD4 antibodies can suppress experimental antiphospholipid syndrome (APS) and systemic lupus erythematosus (SLE) induced by an anti‐DNA monoclonal antibody (MAb).Methods. BALB/c mice were treated with anti‐CD4 MAb either before or 2 months after induction of experimental APS and SLE. Control mice were treated with rat IgG or phosphate buffered saline. Serologic and clinical manifestations of the disease were determined.Results. Treatment of mice with anti‐CD4 before or 2 months after disease induction prevented the development of experimental APS and SLE. The treated mice did not develop leukopenia or proteinuria, and had fewer episodes of fetal resorption. Similarly, the treated mice did not develop elevated erythrocyte sedimentation rate, prolonged activated partial thromboplastin time, or thrombocytopenia, and had significantly lower levels of antibodies to double‐stranded DNA, histones, MIV‐7, cardiolipin, and phosphatidylserine. Levels of CD4+ cells in the lymph nodes declined temporarily after the treatment and then returned to normal.Conclusion. Anti‐CD4 antibodies can prevent experimental APS and SLE. These results may suggest a role for anti‐CD4 treatment in human autoimmune diseases.
Familial polyarteritis nodosa
Authors: Mason Justin C. , Cowie Martin R. , Davies Kevin A. , Schofield John B. , Cambridge Jo , Jackson James , So Alex , Allard Simon A. , Walport Mark J. 
Published: February 2007

AbstractFamilial polyarteritis nodosa (PAN) is rare. We describe here two siblings who developed PAN 8 years apart. HLA typing showed that the affected family members shared a common haplotype with their unaffected mother. Further study of the family history suggested the possibility of an inherited disorder of connective tissue predisposing to autoimmunity and aneurysm formation.
Pyoderma gangrenosum in association with psoriatic arthritis
Authors: Smith David L. , White Clifton R. 
Published: February 2007

AbstractWe present a patient with psoriasis and psoriatic arthritis who developed multiple large, painful ulcers that were scattered over his anterior lower legs and were characteristic of pyoderma gangrenosum (PG). This association has not previously been described. We review other forms of arthritis that usually occur with PG and discuss them in light of this observation.
Therapy for severe interstitial lung disease in systemic sclerosis. a retrospective study
Authors: Steen Virginia D. , Lanz James K. , Conte Claudia , Owens Gregory R. , Medsger Thomas A. 
Published: February 2007

AbstractObjective. This retrospective observational study attempted to determine whether any of the therapies used in the management of systemic sclerosis (SSc) patients held potential benefit for patients with interstitial lung disease.Methods. All patients with SSc who had a pulmonary function test (PFT) showing a forced vital capacity (FVC) of <70% predicted and an additional PFT at least 4 months later were grouped according to the treatment they received. Changes in pulmonary function were analyzed by the mean percent predicted FVC from the initial and the final test, and by the rate of percent change in FVC (ml/year) in the first 2 years after therapy. Bronchoalveolar lavage was performed in a subset of these patients.Results. Of 363 SSc patients who had an FVC < 70% predicted, 122 had a second PFT and fulfilled the criteria for one of the following drug groups: high–dose prednisone (n = 21), immunosuppressive other than cyclophosphamide (CYC) (n = 16), CYC (n = 14), D–penicillamine (n = 37), or no drug (n = 34). In both analyses, the CYC–treated group showed significantly more improvement in FVC than did the other groups. Patients with early disease had the greatest likelihood of responding to any drug.Conclusion. This retrospective study shows that patients treated with CYC had a significant improvement in FVC over time. Prospective controlled studies of CYC treatment in early disease are necessary to determine if it can significantly alter the natural history of interstitial lung disease.
Magnesium deficiency in the eosinophilia—myalgia syndrome. report of clinical and biochemical improvement with repletion
Authors: Clauw Daniel J. , Ward Kathleen , Wilson Beverly , Katz Paul , Rajan Sunder S. 
Published: February 2007

AbstractWe describe a patient with the eosinophilia–myalgia syndrome (EMS) with persistent myalgias, cramping, and weakness that were not responsive to treatment. Despite a normal serum magnesium level, a loading study was performed, and the results suggested low tissue levels of magnesium. He was given parenteral magnesium and had dramatic improvement in symptoms as well as in muscle intracellular levels of this cation. After cessation of magnesium therapy the symptoms recurred, and magnesium repletion again led to an improvement in symptoms and ATP levels. Low tissue levels of magnesium, even in the setting of normal serum levels, may lead to the neuromuscular symptoms in EMS and related disorders.
Antisense oligonucleotides, a novel tool for the control of cytokine effects on human cartilage. focus on interleukins 1 and 6 and proteoglycan synthesis
Authors: Nietfeld J. J. , Duits A. J. , Tilanus M. G. J. , Van Bosch M. E. Den , Den Otter W. , Capel P. J. A. , Bijlsma J. W. J. 
Published: February 2007

AbstractObjective. To prevent the negative effects of interleukin–1 (IL–1) and IL–1—induced IL–6 on cartilage proteoglycan (PG) synthesis, we used an antisense oligonucleotide (ASO) specific for IL–6 messenger RNA (mRNA) to inhibit IL–6 production.Methods. Explants of human articular cartilage were cultured in the presence or absence of IL–6—ASO, IL–1, and exogenous IL–6. As metabolic parameters, cartilage production of IL–6 was determined in the B9 bioassay and PG as incorporation of 35SO4.Results. The IL–6—ASO prevented IL–1—induced production of IL–6 in the cartilage explants, as well as IL–1—induced inhibition of PG synthesis. This inhibition was restored, despite the presence of IL–6—ASO, when exogenous IL–6 was added. A control ASO (not specific for IL–6 mRNA) was not effective.Conclusion. The IL–6—ASO used can penetrate the extracellular matrix of articular cartilage, enter the chondrocytes, and inhibit the IL–1—induced production of IL–6. Furthermore, IL–6—ASO can prevent the IL–1—induced inhibition of cartilage PG synthesis. The effect of exogenous IL–6 shows that IL–1 requires IL–6 for inhibition of PG synthesis.
Lymphocyte function—associated antigen 1 overexpression and t cell autoreactivity
Authors: Richardson Bruce , Powers Daniel , Hooper Forrest , Yung Raymond L. , O'Rourke Kenneth 
Published: February 2007

AbstractObjective. To determine if DNA methylation inhibitors make T cells autoreactive by inducing lymphocyte function—associated antigen type 1 (LFA–1) (CD11a/CD18) overexpression.Methods. T cell clones were treated with 3 distinct DNA methylation inhibitors or were stably transfected with a CD18 cDNA in a mammalian expression vector, and the effects on LFA–1 expression and activation requirements were examined.Results. LFA–1 overexpression, caused by DNA methylation inhibitors or by transfection, correlates with the development of autoreactivity.Conclusion. LFA–1 overexpression may contribute to T cell autoreactivity.
Specificity of autoantibodies for recombinant 60–kd and 52–kd ro autoantigens
Authors: Williams Clair E. ST. , Burch James A. , Saitta Michael 
Published: February 2007

AbstractObjective. To compare patterns of Ro autoantigen recognition in primary Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE).Methods. Sera were tested by enzyme–linked immunosorbent assay (ELISA) and immunoprecipitation for reactivity with recombinant human 60–kd and 52–kd Ro proteins.Results. SLE and primary SS sera exhibited similar patterns of reactivity with the recombinant 52–kd protein. However, a greater proportion of sera from primary SS patients than from SLE patients did not react with recombinant 60–kd protein in ELISA yet precipitated its translation product in solution–phase assays.Conclusion. Disease state can influence recognition of the recombinant 60–kd Ro antigen.
Interleukin–1 receptor antagonist gene polymorphism as a disease severity factor in systemic lupus erythematosus
Authors: Blakemore Alexandra I. F. , Tarlow Joanna K. , J.Cork Michael , Gordon Caroline , Emery Paul , Duff Gordon W. 
Published: February 2007

AbstractObjective. We have previously described associations between an allele of the interleukin–1 receptor antagonist gene (IL1RN) and several inflammatory diseases. In this study we tested the IL1RN gene as a possible marker in patients with systemic lupus erythematosus (SLE).Methods. Eighty–one SLE patients and 261 ethnically matched control subjects were genotyped by polymerase chain reaction.Results. We found an increase in both frequency and carriage rate of IL1RN*2 in the SLE group. This association strengthened with extensive disease and particularly with the presence of photosensitivity and discoid skin lesions.Conclusion. We describe a novel association between IL1RN*2 and SLE. Carriage of the allele seems to influence severity rather than susceptibility to SLE. We postulate that the association of this polymorphism with disease severity is a widespread feature of common inflammatory and autoimmune diseases.
Migration and homing of lymphocytes to lymphoid and synovial tissues in proteoglycan–induced murine arthritis
Authors: Mikecz Katalin , Glant Tibor T, 
Published: February 2007

AbstractObjective. To describe the migration and homing of labeled donor lymphocytes to the lymphoid organs and synovial tissues of host animals, during the development of cartilage proteoglycan (PG)—induced arthritis adoptively transferred to syngeneic BALB/c mice.Methods. Lymphocytes from either nonarthritic or arthritic donor animals were labeled with either fluorescent or radioactive cell linkers (PKH–GL) and injected into syngeneic, immunosuppressed mice. The homing patterns of donor lymphocytes following the injection of labeled cells were studied by fluorescence microscopy and by measurement of radioactivity in tissue samples.Results. Lymphocytes from arthritic donors retained their ability to transfer the disease after labeling. In the lymphoid organs, arthritic and nonarthritic donor lymphocytes exhibited similar homing patterns, although remarkable differences were found in the number of homing cells derived from nonarthritic and arthritic donors. However, labeled cells only from arthritic animals migrated to the synovial tissue of the recipient mice, and their appearance was associated with the onset of arthritis.Conclusion. Lymphocytes from mice with PG–induced arthritis, in contrast to lymphocytes from nonarthritic donors, exhibit preferential homing to the synovial tissue of the host. Adoptive transfer of arthritis is linked to the appearance of these cells in the synovium.
High levels of bcl‐2 protein in circulating t lymphocytes, but not b lymphocytes, of patients with systemic lupus erythematosus
Authors: Aringer Martin , Wintersberger Winfried , Steiner Carl W. , Kiener Hans , Presterl Elisabeth , Jaeger Ulrich , Smolen Josef S. , Graninger Winfried B. 
Published: February 2007

AbstractObjective. Defective regulation of programmed cell death (apoptosis) may play a role in the development of autoimmune diseases, and the proto‐oncogene bcl‐2 is involved in the control of apoptosis in immunocompetent cells. We therefore wished to investigate the expression of bcl‐2 in the peripheral lymphocytes of patients with systemic lupus erythematosus (SLE), a prototypical autoimmune disease.Methods. Levels of bcl‐2 expression in the lymphocytes of patients with SLE and, for comparison, in the lymphocytes of healthy controls and patients with rheumatoid arthritis (RA), systemic bacterial infections, and chronic B cell lymphocytic leukemia were studied by 2‐color cytofluorography and RNA analysis.Results. In SLE patients, a significant proportion of T cells expressed increased amounts of bcl‐2 protein. By fluorescence‐activated cell sorter analysis, bcl‐2‐enriched lymphocytes were found in the CD45RO+ as well as in the CD45RO‐, and also in the CD4+ and CD8+, lymphocyte subpopulations. Mononuclear cells of patients with SLE showed increased amounts of bcl‐2 messenger RNA. An increased percentage of strongly bcl‐2 positive peripheral T lymphocytes was found in patients with bacterial infections, but not in those with RA.Conclusion. Although the occurrence of circulating T lymphocytes with abnormally high bcl‐2 expression is not specific for SLE, it is evidence for a dysregulation of lymphocytic programmed cell death in this autoimmune disease.
Increased frequency of vβ17‐positive t cells in patients with rheumatoid arthritis
Authors: Zagon Gary , Tumang Joseph R. , Li Yixin , Friedman Steven M. , Crow Mary K. 
Published: February 2007

AbstractObjective. To identify the T lymphocytes that mediate disease in rheumatoid arthritis (RA).Methods. A panel of monoclonal antibodies reactive with T cell receptor (TCR) Vβ gene products was used to analyze the RA T cell repertoire.Results. Of 5 TCR Vβ gene products studied, only Vβ17‐positive T cells were increased in peripheral blood and synovial fluid (SF) from RA patients, compared with controls (P < 0.01 and P = 0.0006, respectively). Thirty‐one percent of the 49 RA SF samples and none of the 19 non‐RA SF samples contained >10% Vβ17‐positive T cells. Activated (Tac‐positive) T cells were enriched among Vβ17‐positive synovial T cells.Conclusion. The selective increase of Vβ17‐positive T cells suggests a role for those T cells in the pathogenesis of RA.
β2‐Glycoprotein i reactivity of monoclonal anticardiolipin antibodies from patients with the antiphospholipid syndrome
Authors: Ichikawa Kenji , Khamashta Munther A. , Koike Takao , Matsuura Eiji , Hughes Graham R. V. 
Published: February 2007

AbstractObjective. To elucidate the specificity of anticardiolipin antibodies (aCL) from patients with the antiphospholipid syndrome (APS) to various phospholipids (PLs), DNA, and β2‐glycoprotein I (β2‐GPI).Methods. Five monoclonal aCL were established from peripheral blood lymphocytes of 3 patients with the APS. The reactivity of monoclonal aCL with various PLs, with DNA, and with β2‐GPI was examined by enzyme‐linked immunosorbent assay (ELISA).Results. All of the monoclonal aCL bound to anionic PLs, only in the presence of β2‐GPI. Neither monoclonal aCL nor β2‐GPI bound to DNA. Monoclonal aCL bound to solid‐phase β2‐GPI on polystyrene ELISA plates that had carboxyl groups on their surface, but did not react with solid‐phase β2‐GPI on ordinary polystyrene plates. A mixture of β2‐GPI and CL inhibited the binding of monoclonal aCL to β2‐GPI, but CL or β2‐GPI alone did not.Conclusion. Monoclonal aCL may recognize a cryptic epitope, which appears as a result of β2‐GPI binding to anionic PLs or to polystyrene with carboxyl groups.
Molecular cloning of a soluble form of the granulocyte‐‐macrophage colony‐stimulating factor receptor α chain from a myelomonocytic cell line. expression, biologic activity, and preliminary analysis of transcript distribution
Authors: Williams William V. , Vonfeldt Joan M. , Rosenbaum Helga , Ugen Kenneth E. , Weiner David B. 
Published: February 2007

AbstractObjective. To analyze the molecular and functional characteristics of a soluble form of the granulocytemacrophage colony‐stimulating factor receptor α chain (sGM‐CSFRα), and analyze transcript expression in immune cells and the cellular constituents of rheumatoid arthritis synovial tissue.Methods. We amplified, cloned, and expressed the sGM‐CSFRα and transmembrane form of the receptor (tmGM‐CSFRα) from complementary DNA derived from a human myelomonocytic cell line. Competitive polymerase chain reaction assays were developed to determine the absolute and relative amounts of tmGM‐CSFRα versus sGM‐CSFRα message synthesized by various cell lines and tissues.SResults. sGM‐CSFRα transcripts were detected in bone marrow, monocyte/macrophages (cultured in GM‐CSF), rheumatoid synovial tissue, and rheumatoid synovial tissue T cell lines, and represented the predominant transcript in synovial fibroblasts and osteoarthritis synovial tissue. Levels of expression in monocyte/macrophages and some synovial fibroblast and T cell lines approached those seen in transfected cell lines producing functional sGM‐CSFRα.Conclusion. sGM‐CSFRα represents a functional antagonist of GM‐CSF activity in vitro. Expression of sGM‐CSFRα in bone marrow, rheumatoid synovial tissue T cells, and synovial fibroblasts suggests an important role in vivo, both in regulating myelopoiesis and in modulating the immune response.
The efficacy and toxicity of combination therapy in rheumatoid arthritis. a meta‐analysis
Authors: Felson David T. , Anderson Jennifer J. , Meenan Robert F. 
Published: February 2007

AbstractObjective. To evaluate the efficacy and toxicity of combination therapy, compared with single second‐line drug therapy, in rheumatoid arthritis.Methods. This study was a meta‐analysis of published trials that evaluated combinations of full‐dose second‐line drugs and compared them with single second‐line drugs at full dose. Using a random effects model, we summarized the difference between improvement with combination therapy and improvement with single‐drug therapy.Results. Five trials that met inclusion criteria, which contained 749 entering patients and 516 completing patients, were identified. The mean ± SEM difference in improvement in tender joint count between combination and single‐drug therapy at end of trial (24–52 weeks) was 2.4 ± 0.7 joints (out of 60) (P < 0.001). At end of trial the difference between therapies in swollen joint counts was 1.0 ± 1.2 joints (P = 0.42). The difference in grip strength improvement was 3.7 ± 4.3 mm Hg (P = 0.40), and for erythrocyte sedimentation rate it was 3.4 ± 3.1 mm/hour (P = 0.27). In general, the differences in efficacy between combination and single‐drug therapy were clinically marginal. Nine percent more combination therapy‐treated patients experienced side effect‐related discontinuation of therapy than patients receiving single‐drug therapy (P = 0.008).Conclusion. Combination therapy, as it has been used in recent clinical trials, does not offer a substantial improvement in efficacy, but does have higher toxicity than single drug therapy. These combination therapy regimens are not recommended for widespread use. Other more aggressive regimens with additional drugs or higher drug doses than have been studied might be more efficacious, but with an even higher rate of toxicity.
Effect of hormone replacement therapy on bone mass in rheumatoid arthritis patients treated with and without steroids
Authors: Hall Gerard M. , Daniels Maxine , Doyle David V. , Spector Tim D. 
Published: February 2007

AbstractObjective. To assess the effect of hormone replacement therapy (HRT) on bone mass in rheumatoid arthritis (RA) patients treated with and those not treated with steroids.Methods. Two hundred postmenopausal women with RA (ages 45‐65 years) were randomly allocated to receive transdermal estradiol (hormone replacement therapy; HRT) (50 μg daily) or calcium supplementation (400 mg daily) for 2 years. Forty‐two of the patients (21%) were taking corticosteroids. Bone mineral density of the lumbar spine (BMDLS) and of the proximal femur (BMDF) was measured at study entry and at 12 months and 24 months.Results. In the HRT group overall, mean BMDLS had changed by +2.22% (95% confidence interval [95% CI] +0.72, +3.72) and mean BMDF by −0.41 % (95% CI −1.89, +1.07) after 24 months. In the calcium group, mean BMDLS changed by −1.19% (95% CI −2.29, −0.09) and mean BMDF by −0.56% (95% CI −2.60, +1.48). Differences between treatment groups were significant for the spine only (P < 0.001). In the 21 HRT‐treated patients taking steroids, BMDLS increased by 3.75% (95% CI +0.72, +6.78) and BMDF by 1.62% (95% CI −1.27, +4.51).Conclusion. This study shows that HRT increases spinal BMD and maintains femoral BMD in postmenopausal RA. HRT is also an effective agent in preserving bone mass in patients taking low‐dose corticosteroids.
Somatostatin receptor imaging. the presence of somatostatin receptors in rheumatoid arthritis
Authors: Vanhagen P. M. , Markusse H. M. , Lamberts S. W. J. , Kwekkeboom D. J. , Reubi J. C. , Krenning E. P. 
Published: February 2007

AbstractObjective. To investigate the in vivo and in vitro expression of somatostatin receptors (SS‐R) on synovial membranes of patients with rheumatoid arthritis (RA).Methods. The joints of 14 consecutive patients with active RA, 4 patients with severe osteoarthritis (OA), and 30 control patients were studied. The somatostatin analog [111In‐DTPA‐D‐Phe1]‐octreotide was used for in vivo SS‐R scintigraphy, and the somatostatin analog [125I‐Tyr3]‐octreotide for in vitro SS‐R autoradiography.Results. Seventy‐six percent (220 of 290) of the painful joints and 76% (207 of 274) of the swollen joints of the patients with RA were visualized by SS‐R scintigraphy. The degree of pain and swelling correlated well with positive scintigraphy findings in the joints (P < 0.0001). In 2 of the RA patients who underwent scintigraphy, as well as in 4 of 5 other patients, in vitro studies of the synovial membranes showed the presence of specific SS‐R. In patients with OA, uptake of radioactivity in the affected joints was significantly lower than that in patients with RA. None of the joints of the control patients demonstrated uptake of radioactivity.Conclusion. SS‐R are present in the synovial tissue of patients with active RA, as demonstrated by both in vivo and in vitro techniques. The potential value of SS‐R scintigraphy in the clinical evaluation of patients with active RA is presently unknown.