248 results match your criteria Arthritis research[Journal]


21st European Workshop for Rheumatology Research, Vienna, Austria, 1-4 March 2001. Abstracts.

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Arthritis Res 2001 9;3 Suppl A:A1-47. Epub 2001 Feb 9.

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Effects of disease modifying agents and dietary intervention on insulin resistance and dyslipidemia in inflammatory arthritis: a pilot study.

Arthritis Res 2002 16;4(6):R12. Epub 2002 Sep 16.

Department of Rheumatology, Johannesburg Hospital, University of the Witwatersrand, South Africa.

Patients with rheumatoid arthritis (RA) experience excess cardiovascular disease (CVD). We investigated the effects of disease-modifying antirheumatic drugs (DMARD) and dietary intervention on CVD risk in inflammatory arthritis. Twenty-two patients (17 women; 15 with RA and seven with spondyloarthropathy) who were insulin resistant (n = 20), as determined by the Homeostasis Model Assessment, and/or were dyslipidemic (n = 11) were identified. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153842PMC
http://dx.doi.org/10.1186/ar597DOI Listing

Angiogenic and angiostatic factors in systemic sclerosis: increased levels of vascular endothelial growth factor are a feature of the earliest disease stages and are associated with the absence of fingertip ulcers.

Arthritis Res 2002 30;4(6):R11. Epub 2002 Aug 30.

Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Switzerland.

To examine whether the lack of sufficient neoangiogenesis in systemic sclerosis (SSc) is caused by a decrease in angiogenic factors and/or an increase in angiostatic factors, the potent proangiogenic molecules vascular endothelial growth factor (VEGF) and basic fibroblast growth factor, and the angiostatic factor endostatin were determined in patients with SSc and in healthy controls. Forty-three patients with established SSc and nine patients with pre-SSc were included in the study. Serum levels of VEGF, basic fibroblast growth factor and endostatin were measured by ELISA. Read More

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http://arthritis-research.biomedcentral.com/articles/10.1186
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153841PMC
http://dx.doi.org/10.1186/ar596DOI Listing
April 2003
1 Read

VLA-4-dependent and -independent pathways in cell contact-induced proinflammatory cytokine production by synovial nurse-like cells from rheumatoid arthritis patients.

Arthritis Res 2002 12;4(6):R10. Epub 2002 Aug 12.

Laboratory of Molecular and Cellular Recognition, Osaka University Graduate School of Medicine, Japan.

Nurse-like stromal cell lines from the synovial tissue of patients with rheumatoid arthritis (RA-SNC) produce, on coculture with lymphocytes, large amounts of proinflammatory cytokines. In the present paper, we analyze the molecular events necessary for the induction of cytokine release from RA-SNC cells, and particularly the roles played by cell adhesion and the transmigration (also known as pseudoemperipolesis) of lymphocytes. For this purpose, the effects of various mAbs on the binding and transmigration of a human B-cell line, MC/car, were examined using a cloned RA-SNC line, RA-SNC77. Read More

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http://arthritis-research.biomedcentral.com/articles/10.1186
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153839PMC
http://dx.doi.org/10.1186/ar593DOI Listing
April 2003
2 Reads

Abnormalities of B cell phenotype, immunoglobulin gene expression and the emergence of autoimmunity in Sjögren's syndrome.

Arthritis Res 2002 25;4(6):360-71. Epub 2002 Sep 25.

Department of Medicine, Rheumatology and Clinical Immunology, University Hospital Charité, Berlin, Germany.

Primary Sjögren's syndrome (pSS) is an autoimmune disorder characterized by specific pathologic features and the production of typical autoantibodies. In addition, characteristic changes in the distribution of peripheral B cell subsets and differences in use of immunoglobulin variable-region genes are also features of pSS. Comparison of B cells from the blood and parotid gland of patients with pSS with those of normal donors suggests that there is a depletion of memory B cells from the peripheral blood and an accumulation or retention of these antigen-experienced B cells in the parotids. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153845PMC
http://dx.doi.org/10.1186/ar603DOI Listing

Genetic aspects of Sjögren's syndrome.

Arthritis Res 2002 24;4(6):353-9. Epub 2002 Sep 24.

Broegelmann Research Laboratory, Department of Microbiology and Immunology, The Gade Institute, University of Bergen, Norway.

Sjögren's syndrome is a multisystem inflammatory rheumatic disease that is classified into primary and secondary forms, with cardinal features in the eye (keratoconjunctivitis sicca) and mouth (xerostomia). The aetiology behind this autoimmune exocrinopathy is probably multifactorial and influenced by genetic as well as by environmental factors that are as yet unknown. A genetic predisposition to Sjögren's syndrome has been suggested on the basis of familial aggregation, animal models and candidate gene association studies. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153844PMC
http://dx.doi.org/10.1186/ar599DOI Listing
April 2003
2 Reads

Interferon-beta for treatment of rheumatoid arthritis?

Arthritis Res 2002 18;4(6):346-52. Epub 2002 Sep 18.

Division of Clinical Immunology and Rheumatology Academic Medical Center, University of Amsterdam, The Netherlands.

IFN-beta treatment is emerging as a potentially effective form of therapy in various immune-mediated conditions. The present review addresses the possible role of IFN-beta in immune-mediated diseases such as multiple sclerosis and rheumatoid arthritis. Several placebo-controlled trials are discussed, as are the available immunological data that are relevant to this field. Read More

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http://arthritis-research.biomedcentral.com/articles/10.1186
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153843PMC
http://dx.doi.org/10.1186/ar598DOI Listing
April 2003
4 Reads

The role of structural genes in the pathogenesis of osteoarthritic disorders.

Arthritis Res 2002 30;4(6):337-45. Epub 2002 Aug 30.

Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.

Osteoarthritis (OA), one of the most common age-related chronic disorders of articular cartilage, joints, and bone tissue, represents a major public health problem. Genetic studies have identified multiple gene variations associated with an increased risk of OA. These findings suggest that there is a large genetic component to OA and that the disorder belongs in the multigenetic, multifactorial class of genetic diseases. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153840PMC
http://dx.doi.org/10.1186/ar595DOI Listing
April 2003
4 Reads

Paradoxical roles of IFN-gamma in models of Th1-mediated autoimmunity.

Arthritis Res 2002 17;4(6):333-6. Epub 2002 Jul 17.

VA Medical Center, Research Service (151), Memphis, Tennessee, USA.

T-cell responses to antigens are classified on the basis of the cytokines they produce as either Th1 (IFN-gamma, IL-2) or Th2 (IL-4, IL-10), with these Th types being indicative of either cell-mediated or antibody-mediated responses, respectively. Using this classification, T-cell responses in MHC-class-II-restricted autoimmune diseases appear to be predominantly of the Th1 type, based on the presence of high levels of IFN-gamma. This simplistic classification has recently been challenged, however, as disease incidence and severity are frequently elevated in animals that have a deficient IFN-gamma response. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC153838PMC
http://dx.doi.org/10.1186/ar432DOI Listing

Regulation of CD154-induced interleukin-12 production in synovial fluid macrophages.

Arthritis Res 2002 26;4(5):R9. Epub 2002 Jul 26.

Turku Graduate School of Biomedical Sciences, Turku University, Finland.

Interleukin (IL)-12, being a major cytokine that induces T helper (Th) 1 differentiation and inflammatory response, has been postulated to be an important mediator of synovial inflammation in rheumatoid arthritis (RA). However, the regulation of IL-12 production in RA has not been elucidated. Our knowledge is mainly based on studies of the production of IL-12p40 and not the functional IL-12p70 heterodimer. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061561PMC
http://dx.doi.org/10.1186/ar589DOI Listing
February 2003

Molecular profile of synovial fibroblasts in rheumatoid arthritis depends on the stage of proliferation.

Arthritis Res 2002 17;4(5):R8. Epub 2002 Jul 17.

Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zürich, Gloriastrasse 25, Switzerland.

The aim of this study was to explore the molecular profile of proliferating rheumatoid arthritis synovial fibroblasts (RA-SF). Total RNA was extracted from two cultures of RA-SF (low-density [LD] proliferating cells and high-density [HD] nonproliferating cells) and suppression subtractive hybridization was performed to compare differential gene expression of these two cultures. Subtracted cDNA was subcloned, and nucleotide sequences were analyzed to identify each clone. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC125298PMC
http://dx.doi.org/10.1186/ar427DOI Listing
February 2003
21 Reads

Anti-TNF-alpha antibody allows healing of joint damage in polyarthritic transgenic mice.

Arthritis Res 2002 28;4(5):R7. Epub 2002 Jun 28.

Centocor, Inc, Malvern, Pennsylvania, USA.

Anti-tumor-necrosis-factor-alpha (TNF-alpha) monoclonal antibody was used to treat Tg197 transgenic mice, which constitutively produce human TNF-alpha (hTNF-alpha) and develop a progressive polyarthritic disease. Treatment of both young (7- or 8-week-old) and aged (27- or 28-week-old) mice commenced when at least two limbs showed signs of moderate to severe arthritis. The therapeutic efficacy of anti-TNF-alpha antibody was assessed using various pathological indicators of disease progression. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC125301PMC
http://dx.doi.org/10.1186/ar430DOI Listing
February 2003
2 Reads

Lack of autoantibody production associated with cytomegalovirus infection.

Arthritis Res 2002 20;4(5):R6. Epub 2002 Jun 20.

Department of Pediatrics, Virginia Commonwealth University/Medical College of Virginia, Richmond, USA.

To confirm an association between cytomegalovirus (CMV) infection and the presence of antibodies to Smith (Sm), to ribonucleoprotein (RNP), and to a component of the U1 ribonucleoproteins (U1-70 kD), we measured antibodies to these protein antigens using an enzyme immunoassay and an immunoblot. The antibodies were measured in the sera of 80 healthy subjects, one-half of whom were naturally CMV seropositive and one-half were CMV seronegative, and in eight subjects immunized with a live attenuated strain of CMV. None of the vaccinees developed antibodies to Sm, to RNP, or to U1-70 kD at either 4 or 12 months after immunization. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC125300PMC
http://dx.doi.org/10.1186/ar429DOI Listing
February 2003

Cardiovascular risk in rheumatoid arthritis versus osteoarthritis: acute phase response related decreased insulin sensitivity and high-density lipoprotein cholesterol as well as clustering of metabolic syndrome features in rheumatoid arthritis.

Arthritis Res 2002 19;4(5):R5. Epub 2002 Jun 19.

Department of Rheumatology, Johannesburg Hospital, University of the Witwatersrand, South Africa.

Rheumatoid arthritis (RA) patients experience a markedly increased frequency of cardiovascular disease. We evaluated cardiovascular risk profiles in 79 RA patients and in 39 age-matched and sex-matched osteoarthritis (OA) patients. Laboratory tests comprised ultrasensitive C-reactive protein (CRP) and fasting lipids. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC125299PMC
http://dx.doi.org/10.1186/ar428DOI Listing
February 2003
1 Read

To keep the catch - that is the question: a personal account of the 3rd Annual EULAR Congress, Stockholm.

Authors:
Frank A Wollheim

Arthritis Res 2002 ;4(5):E007

Department of Rheumatology, Lund University Hospital, Lund, Sweden.

The 3rd Annual EULAR Congress, held in Stockholm on 12-15 June 2002, had a turnout of 8300 delegates, almost identical to last year's record attendance level in Prague. The venue was close to ideal, allowing ample space for poster sessions in the exhibition hall. The manned poster sessions were well attended, even on the last day of the Congress. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC128936PMC
http://dx.doi.org/10.1186/ar424DOI Listing
February 2003

Genetics of osteoarticular disorders, Florence, Italy, 22-23 February 2002.

Arthritis Res 2002 30;4(5):326-31. Epub 2002 Jul 30.

Department of Internal Medicine, University of Florence, Italy.

Osteoporosis (OP) and osteoarthritis (OA), the two most common age-related chronic disorders of articular joints and skeleton, represent a major public health problem in most developed countries. They are influenced by environmental factors and exhibit a strong genetic component. Large population studies clearly show their inverse relationship; therefore, an accurate analysis of the genetic bases of one of these two diseases may provide data of interest for the other disorder. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC128940PMC
http://dx.doi.org/10.1186/ar590DOI Listing
February 2003
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Therapy of ankylosing spondylitis and other spondyloarthritides: established medical treatment, anti-TNF-alpha therapy and other novel approaches.

Arthritis Res 2002 6;4(5):307-21. Epub 2002 Aug 6.

Rheumazentrum Ruhrgebiet, Herne, Germany.

Therapeutic options for patients with more severe forms of spondyloarthritis (SpA) have been rather limited in recent decades. There is accumulating evidence that anti-tumor-necrosis-factor (anti-TNF) therapy is highly effective in SpA, especially in ankylosing spondylitis and psoriatic arthritis. The major anti-TNF-alpha agents currently available, infliximab (Remicade(R)) and etanercept (Enbrel(R)), are approved for the treatment of rheumatoid arthritis (RA) in many countries. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC128942PMC
http://dx.doi.org/10.1186/ar592DOI Listing
February 2003
5 Reads

Juvenile idiopathic arthritis genetics - what's new? What's next?

Arthritis Res 2002 5;4(5):302-6. Epub 2002 Aug 5.

Arthritis Research Campaign Epidemiology Unit, School of Epidemiology and Health Sciences, University of Manchester, Stopford Building, Oxford Road, UK.

Studies have established the magnitude of the genetic basis of juvenile idiopathic arthritis (JIA). JIA is a complex genetic condition and the genes that influence susceptibility are actively being sought. A candidate gene approach is being used by several groups. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC128941PMC
http://dx.doi.org/10.1186/ar591DOI Listing
February 2003
3 Reads

Cartilage-specific autoimmunity in animal models and clinical aspects in patients - focus on relapsing polychondritis.

Arthritis Res 2002 17;4(5):296-301. Epub 2002 Jul 17.

Department of Clinical Immunology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Relapsing polychondritis is an autoimmune disease in which an inappropriate immune response destroys cartilage. Cartilage of the ears, larynx and nose rather than spine and joint cartilage is affected by a chronic relapsing and erosive inflammation. Several animal models for relapsing polychondritis have been published in which immunization with various cartilage proteins induces a variety of chondritis symptoms that mimic those seen in patients. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC128937PMC
http://dx.doi.org/10.1186/ar425DOI Listing
February 2003
4 Reads

Autoantibody profiling for the study and treatment of autoimmune disease.

Arthritis Res 2002 7;4(5):290-5. Epub 2002 May 7.

Department of Medicine, Division of Rheumatology and Immunology, Stanford University School of Medicine, California, USA.

Proteomics technologies enable profiling of autoantibody responses using biological fluids derived from patients with autoimmune disease. They provide a powerful tool to characterize autoreactive B-cell responses in diseases including rheumatoid arthritis, multiple sclerosis, autoimmune diabetes, and systemic lupus erythematosus. Autoantibody profiling may serve purposes including classification of individual patients and subsets of patients based on their 'autoantibody fingerprint', examination of epitope spreading and antibody isotype usage, discovery and characterization of candidate autoantigens, and tailoring antigen-specific therapy. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC128938PMC
http://dx.doi.org/10.1186/ar426DOI Listing
February 2003
1 Read

The molecular mechanism of osteoclastogenesis in rheumatoid arthritis.

Arthritis Res 2002 12;4(5):281-9. Epub 2002 Apr 12.

Department of Biochemistry, Matsumoto Dental University, Nagano, Japan.

Bone-resorbing osteoclasts are formed from hemopoietic cells of the monocyte-macrophage lineage under the control of bone-forming osteoblasts. We have cloned an osteoblast-derived factor essential for osteoclastogenesis, the receptor activator of NF-kappaB ligand (RANKL). Synovial fibroblasts and activated T lymphocytes from patients with rheumatoid arthritis also express RANKL, which appears to trigger bone destruction in rheumatoid arthritis as well. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC128939PMC
http://dx.doi.org/10.1186/ar431DOI Listing
February 2003

Emerging role of anti-tumor necrosis factor therapy in rheumatic diseases.

Authors:
Joachim R Kalden

Arthritis Res 2002 24;4 Suppl 2:S34-40. Epub 2002 May 24.

Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen-Nurnberg, Erlangen, Germany.

Tumor necrosis factor alpha (TNF-alpha) is an inflammatory cytokine that has been implicated in a variety of rheumatic and inflammatory diseases. New understanding of the importance of TNF-alpha in the pathophysiology of rheumatoid arthritis and Crohn's disease led to the development of a new class of targeted anti-TNF therapies. Anti-TNF-alpha agents including etanercept (a fusion protein of the p75 TNF receptor and IgG1) and infliximab (a chimeric monoclonal antibody specific for TNF-alpha) have been approved for the treatment of rheumatoid arthritis. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3238220PMC
http://dx.doi.org/10.1186/ar552DOI Listing

Structural damage in rheumatoid arthritis as visualized through radiographs.

Arthritis Res 2002 27;4 Suppl 2:S29-33. Epub 2002 Mar 27.

University Hospital Maastricht, Maastricht, The Netherlands.

Several agents show an effect on reducing radiographic progression in rheumatoid arthritis. It is tempting to retrospectively compare the effects of these agents on radiographic progression across clinical trials. However, there are several limitations in interpreting and comparing radiographic results across clinical trials. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3238218PMC
http://dx.doi.org/10.1186/ar550DOI Listing
August 2007
2 Reads

How does infliximab work in rheumatoid arthritis?

Arthritis Res 2002 27;4 Suppl 2:S22-8. Epub 2002 Mar 27.

The Kennedy Institute of Rheumatology Division, Imperial College of Science Technology and Medicine, London, UK.

Since the initial characterization of tumor necrosis factor alpha (TNFalpha), it has become clear that TNFalpha has diverse biologic activity. The realization that TNFalpha plays a role in rheumatoid arthritis (RA) has led to the development of anti-TNF agents for the treatment of RA. Infliximab, a chimeric monoclonal antibody that specifically, and with high affinity, binds to TNFalpha and neutralizes the cytokine, is currently approved for the treatment of RA and Crohn's disease, another immune-inflammatory disorder. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3238217PMC
http://dx.doi.org/10.1186/ar549DOI Listing
August 2007
1 Read

Current and future management approaches for rheumatoid arthritis.

Arthritis Res 2002 27;4 Suppl 2:S16-21. Epub 2002 Mar 27.

Leiden University Medical Center, Leiden, The Netherlands.

With the introduction of new disease-modifying antirheumatic drugs (DMARDs) and other therapeutic agents, the management of rheumatoid arthritis (RA) has shifted toward earlier, more aggressive therapy. The ultimate goal is to prevent structural joint damage that leads to pain and functional disability. Early diagnosis of RA is therefore essential, and early DMARD treatment combined with nonsteroidal anti-inflammatory drugs is recommended. Read More

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http://arthritis-research.biomedcentral.com/articles/10.1186
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3238216PMC
http://dx.doi.org/10.1186/ar548DOI Listing
August 2007
2 Reads

The determination and measurement of functional disability in rheumatoid arthritis.

Authors:
Frederick Wolfe

Arthritis Res 2002 8;4 Suppl 2:S11-5. Epub 2002 Apr 8.

National Data Bank for Rheumatic Diseases-Arthritis Research Center Foundation and University of Kansas School of Medicine, Wichita, Kansas, USA.

Although functional outcome is frequently discussed and written about, it is often not clear what functional outcome is and how it can be measured. This paper introduces the concept of latent and observed measures of functional disability, and distinguishes between disability as a process measure and disability as an outcome measure. Using the Health Assessment Questionnaire as the main functional outcome measure in rheumatoid arthritis, we propose and discuss several methods for determining disability, and describe the implications of altering the disability course. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3238215PMC
http://dx.doi.org/10.1186/ar547DOI Listing

Magnetic resonance imaging: opportunities for rheumatoid arthritis disease assessment and monitoring long-term treatment outcomes.

Authors:
Paul Emery

Arthritis Res 2002 18;4 Suppl 2:S6-10. Epub 2002 Apr 18.

Department of Rheumatology, University of Leeds, Leeds, UK.

Early diagnosis of rheumatoid arthritis (RA) combined with early initiation of an appropriate treatment regimen is acknowledged as an important factor in improving clinical outcomes in patients with RA. Early diagnosis allows treatment intervention to occur sooner in order to inhibit the progression of structural joint damage as well as providing improved patient quality of life. Unfortunately, early diagnosis has been challenging due to the non-specific signs and symptoms associated with many polyarthropathies and the lack of accurate definitive diagnostic tests that can accurately classify RA at presentation. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3238221PMC
http://dx.doi.org/10.1186/ar553DOI Listing

Autoantibodies in rheumatoid arthritis and their clinical significance.

Arthritis Res 2002 26;4 Suppl 2:S1-5. Epub 2002 Apr 26.

Vienna General Hospital, University of Vienna, and Ludwig Boltzmann Institute for Rheumatology, Vienna, Austria.

Autoantibodies are proven useful diagnostic tools for a variety of rheumatic and non-rheumatic autoimmune disorders. However, a highly specific marker autoantibody for rheumatoid arthritis (RA) has not yet been determined. The presence of rheumatoid factors is currently used as a marker for RA. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3238219PMC
http://dx.doi.org/10.1186/ar551DOI Listing

Why do we not have a cure for rheumatoid arthritis?

Arthritis Res 2002 9;4 Suppl 3:S297-301. Epub 2002 May 9.

Intramural Research Program, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA.

There are currently unprecedented opportunities to treat rheumatoid arthritis using well-designed, highly effective, targeted therapies. This will result in a substantial improvement in the outcome of this disorder for most affected individuals, if they can afford these therapies. Yet our lack of understanding of the basic mechanisms that initiate and sustain this disease remains a major obstacle in the search for a definitive cure. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240144PMC
http://dx.doi.org/10.1186/ar568DOI Listing

Complement and systemic lupus erythematosus.

Authors:
Mark J Walport

Arthritis Res 2002 9;4 Suppl 3:S279-93. Epub 2002 May 9.

Division of Medicine, Imperial College of Science, Technology and Medicine, London, UK.

Complement is implicated in the pathogenesis of systemic lupus erythematosus (SLE) in several ways and may act as both friend and foe. Homozygous deficiency of any of the proteins of the classical pathway is causally associated with susceptibility to the development of SLE, especially deficiency of the earliest proteins of the activation pathway. However, complement is also implicated in the effector inflammatory phase of the autoimmune response that characterizes the disease. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240161PMC
http://dx.doi.org/10.1186/ar586DOI Listing
May 2003
1 Read

Single nucleotide polymorphisms and disease gene mapping.

Authors:
John I Bell

Arthritis Res 2002 9;4 Suppl 3:S273-8. Epub 2002 May 9.

Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, UK.

Single nucleotide polymorphisms are the most important and basic form of variation in the genome, and they are responsible for genetic effects that produce susceptibility to most autoimmune diseases. The rapid development of databases containing very large numbers of single nucleotide polymorphisms, and the characterization of haplotypes and patterns of linkage disequilibrium throughout the genome, provide a unique opportunity to advance association strategies in common disease rapidly over the next few years. Only the careful use of these strategies and a clear understanding of their statistical limits will allow novel genetic determinants for many of the common autoimmune diseases to be determined. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240131PMC
http://dx.doi.org/10.1186/ar555DOI Listing

Epidemiology and genetics of rheumatoid arthritis.

Arthritis Res 2002 9;4 Suppl 3:S265-72. Epub 2002 May 9.

ARC Epidemiology Unit, School of Epidemiology & Health Sciences, University of Manchester, UK.

The prevalence of rheumatoid arthritis (RA) is relatively constant in many populations, at 0.5-1.0%. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240153PMC
http://dx.doi.org/10.1186/ar578DOI Listing
May 2003
4 Reads

Susceptibility genes in the pathogenesis of murine lupus.

Arthritis Res 2002 9;4 Suppl 3:S255-63. Epub 2002 May 9.

Center for Immunology, University of Texas Southwestern Medical Center, Dallas 75290, USA.

Systemic lupus erythematosus (SLE) is the paradigm of a multisystem autoimmune disease in which genetic factors strongly influence susceptibility. Through genome scans and congenic dissection, numerous loci associated with lupus susceptibility have been defined and the complexity of the inheritance of this disease has been revealed. In this review, we provide a brief description of animal models of SLE, both spontaneous models and synthetic models, with an emphasis on the B6 congenic model derived from analyses of the NZM2410 strain. Read More

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http://arthritis-research.biomedcentral.com/articles/10.1186
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240158PMC
http://dx.doi.org/10.1186/ar583DOI Listing
May 2003
1 Read

Signaling for survival and apoptosis in the immune system.

Arthritis Res 2002 9;4 Suppl 3:S243-52. Epub 2002 May 9.

Ontario Cancer Institute and Department of Medical Biophysics, University of Toronto, Ontario, Canada.

Signal transduction induced by tumor necrosis factor (TNF) family members and their receptors has been an intensive area of research for several years. The major impact of these studies has been the delineation of apoptotic and cell survival signaling pathways. These discoveries, coupled with major advances in the study of mammalian apoptotic machinery, constitute a promising blueprint of the molecular network governing the fate of all living cells. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240145PMC
http://dx.doi.org/10.1186/ar569DOI Listing
May 2003
2 Reads

The paradigm of IL-6: from basic science to medicine.

Arthritis Res 2002 9;4 Suppl 3:S233-42. Epub 2002 May 9.

Department of Molecular Medicine, Osaka University Graduate School of Medicine, Japan.

IL-6 is a pleiotropic cytokine with a wide range of biological activities in immune regulation, hematopoiesis, inflammation, and oncogenesis. Its activities are shared by IL-6-related cytokines such as leukemia inhibitory factor and oncostatin M. The pleiotropy and redundancy of IL-6 functions have been identified by using a unique receptor system comprising two functional proteins: an IL-6 receptor (IL-6R) and gp130, the common signal transducer of cytokines related to IL-6. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240141PMC
http://dx.doi.org/10.1186/ar565DOI Listing

Signaling crosstalk between RANKL and interferons in osteoclast differentiation.

Arthritis Res 2002 9;4 Suppl 3:S227-32. Epub 2002 May 9.

Department of Immunology, Faculty of Medicine and Graduate School of Medicine, University of Tokyo, Japan.

Regulation of osteoclast differentiation is an aspect central to the understanding of the pathogenesis and the treatment of bone diseases such as autoimmune arthritis and osteoporosis. In fact, excessive signaling by RANKL (receptor activator of nuclear factor kappaB ligand), a member of the tumor necrosis factor (TNF) family essential for osteoclastogenesis, may contribute to such pathological conditions. Here we summarize our current work on the negative regulation of osteoclastogenesis by unique signaling crosstalk between RANKL and interferons (IFNs). Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240156PMC
http://dx.doi.org/10.1186/ar581DOI Listing

High-efficiency gene transfer into nontransformed cells: utility for studying gene regulation and analysis of potential therapeutic targets.

Arthritis Res 2002 9;4 Suppl 3:S215-25. Epub 2002 May 9.

Kennedy Institute of Rheumatology Division, Imperial College Faculty of Medicine, London, UK.

The elucidation of the signalling pathways involved in inflammatory diseases, such as rheumatoid arthritis, could provide long sought after targets for therapeutic intervention. Gene regulation is complex and varies depending on the cell type, as well as the signal eliciting gene activation. However, cells from certain lineages, such as macrophages, are specialised to degrade exogenous material and consequently do not easily transfect. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240136PMC
http://dx.doi.org/10.1186/ar560DOI Listing
May 2003
7 Reads

Studies of T-cell activation in chronic inflammation.

Authors:
Andrew P Cope

Arthritis Res 2002 9;4 Suppl 3:S197-211. Epub 2002 May 9.

The Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College, London, UK.

The strong association between specific alleles encoded within the MHC class II region and the development of rheumatoid arthritis (RA) has provided the best evidence to date that CD4+ T cells play a role in the pathogenesis of this chronic inflammatory disease. However, the unusual phenotype of synovial T cells, including their profound proliferative hyporesponsiveness to TCR ligation, has challenged the notion that T-cell effector responses are driven by cognate cartilage antigens in inflamed synovial joints. The hierarchy of T-cell dysfunction from peripheral blood to inflamed joint suggests that these defects are acquired through prolonged exposure to proinflammatory cytokines such as tumour necrosis factor (TNF)-alpha. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240133PMC
http://dx.doi.org/10.1186/ar557DOI Listing

How are the regulators regulated? The search for mechanisms that impose specificity on induction of cell death and NF-kappaB activation by members of the TNF/NGF receptor family.

Arthritis Res 2002 9;4 Suppl 3:S189-96. Epub 2002 May 9.

Department of Biological Chemistry, Weizmann Institute of Science, Rehovot, Israel.

Signals emanating from receptors of the tumor necrosis factor/nerve growth factor (TNF/NGF) family control practically all aspects of immune defense and, as such, constitute potential targets for therapeutic intervention through rational drug design. Indeed, arrest of these signals by blocking ligand-receptor interactions enables effective suppression of a variety of activities that are implicated in various pathologies, such as T and B lymphocyte activation and growth, inflammation, fibroblast proliferation, and cell death. To be therapeutically useful, however, inhibition of signaling should be restricted by determinants of specificity, at least to the same degree observed when blocking activation of individual receptors. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240160PMC
http://dx.doi.org/10.1186/ar585DOI Listing
May 2003
6 Reads

Chemokine receptors on dendritic cells promote autoimmune reactions.

Arthritis Res 2002 9;4 Suppl 3:S183-8. Epub 2002 May 9.

Laboratory of Molecular Immunoregulation, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA.

This paper presents a brief review of several lines of evidence suggesting that chemokine receptors on dendritic cells play an important role in breaking tolerance to self and in inducing autoimmunity. First, we have shown that an idiotypic self-antigen obtained from malignant murine lymphomas, when covalently linked to selected chemokines or defensins that interact with receptors on immature dendritic cells (iDCs), has the capacity to break tolerance to self and induce humoral or cell-mediated anti-tumor responses. Since unlinked antigens mixed with the same chemokines or defensins or antigens fused with a mutant ligand deficient in receptor-binding capacity were not immunogenic, we propose that delivery of an antigen coupled to a ligand for receptors on iDCs promotes the processing and subsequent presentation of the antigen, resulting in immunoadjuvant effects. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240150PMC
http://dx.doi.org/10.1186/ar574DOI Listing
May 2003
16 Reads

Cytokine regulation in RA synovial tissue: role of T cell/macrophage contact-dependent interactions.

Arthritis Res 2002 9;4 Suppl 3:S177-82. Epub 2002 May 9.

Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College of Science, Technology and Medicine, London, UK.

Several groups have documented the expression of cytokines in rheumatoid arthritis synovial tissue over the past 15 years or so. These studies have indicated that most cytokines examined are expressed at the mRNA levels at least, and many other cytokines are found in abundance as proteins. Our attention has recently focused on the mechanisms that induce and regulate tumour necrosis factor and IL-10. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240132PMC
http://dx.doi.org/10.1186/ar556DOI Listing
May 2003
3 Reads

The role of human T-lymphocyte-monocyte contact in inflammation and tissue destruction.

Arthritis Res 2002 9;4 Suppl 3:S169-76. Epub 2002 May 9.

Division of Immunology and Allergy, Clinical Immunology Unit, University Hospital, Geneva, Switzerland.

Contact-mediated signaling of monocytes by human stimulated T lymphocytes (TL) is a potent proinflammatory mechanism that triggers massive upregulation of the proinflammatory cytokines IL-1 and tumor necrosis factor-alpha. These two cytokines play an important part in chronic destructive diseases, including rheumatoid arthritis. To date this cell-cell contact appears to be a major endogenous mechanism to display such an activity in monocyte-macrophages. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240134PMC
http://dx.doi.org/10.1186/ar558DOI Listing
May 2003
3 Reads
28 Citations

The contrasting roles of IL-2 and IL-15 in the life and death of lymphocytes: implications for the immunotherapy of rheumatological diseases.

Authors:
Thomas Waldmann

Arthritis Res 2002 9;4 Suppl 3:S161-7. Epub 2002 May 9.

Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.

Interleukin-15 (IL-15) is a 14-15-kDa member of the 4alpha helix bundle family of cytokines that stimulate T and NK (natural killer) cells. IL-15 and IL-2 utilize heterotrimeric receptors that include the cytokine-specific private receptors IL-2Ralpha and IL-15Ralpha, as well as two receptor elements that they share, IL-2Rbeta and gammac. Although IL-2 and IL-15 share two receptor subunits and many functions, at times they provide contrasting contributions to T-cell-mediated immune responses. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240159PMC
http://dx.doi.org/10.1186/ar584DOI Listing

HLA-B27: natural function and pathogenic role in spondyloarthritis.

Arthritis Res 2002 9;4 Suppl 3:S153-8. Epub 2002 May 9.

MRC Human Immunology Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK.

The human leukocyte antigen HLA-B27 is strongly associated with development of a group of inflammatory arthritides collectively known as the spondyloarthritides. We have set out to define the natural immunological function of HLA-B27, and then to apply this knowledge to understand its pathogenic role. Human leukocyte antigen class 1 molecules bind antigenic peptides for cell surface presentation to cytotoxic T lymphocytes. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240147PMC
http://dx.doi.org/10.1186/ar571DOI Listing
May 2003
1 Read

Multiple roles for tumor necrosis factor-alpha and lymphotoxin alpha/beta in immunity and autoimmunity.

Arthritis Res 2002 9;4 Suppl 3:S141-52. Epub 2002 May 9.

Department of Microbiology and Immunology, Stanford University Medical Center, California 94305, USA.

Tumor necrosis factor (TNF)-alpha and lymphotoxin (LT) alpha/beta play multiple roles in the development and function of the immune system. This article focuses on three important aspects of the effects of these cytokines on the immune response and on autoimmunity. In several experimental systems (Jurkat T cells, murine T-cell hybridomas), TNF-alpha appears to cause a downregulation of signaling through the TCR, revealed by changes in calcium flux, activation of p21, p23 and ZAP70, and a decrease in nuclear activation of NF-kappaB. Read More

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http://arthritis-research.biomedcentral.com/articles/10.1186
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240146PMC
http://dx.doi.org/10.1186/ar570DOI Listing
May 2003
10 Reads

Humanized mice as a model for rheumatoid arthritis.

Arthritis Res 2002 9;4 Suppl 3:S133-40. Epub 2002 May 9.

Department of Microbiology and Immunology, Stanford University School of Medicine, California 94305, USA.

Genetic susceptibility to rheumatoid arthritis (RA), a common autoimmune disease, is associated with certain HLA-DR4 alleles. Treatments are rarely curative and are often tied to major side effects. We describe the development of a humanized mouse model wherein new, less toxic, vaccine-like treatments for RA might be pretested. Read More

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http://arthritis-research.biomedcentral.com/articles/10.1186
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240155PMC
http://dx.doi.org/10.1186/ar580DOI Listing
May 2003
8 Reads

The instructive role of dendritic cells on T-cell responses.

Arthritis Res 2002 9;4 Suppl 3:S127-32. Epub 2002 May 9.

Institute for Research in Biomedicine, Bellinzona, Switzerland.

Immune responses are initiated in the T-cell areas of secondary lymphoid organs where naïve T lymphocytes encounter dendritic cells (DCs) that present antigens taken up in peripheral tissues. DCs represent the interface between the universe of foreign and tissue-specific antigens and T lymphocytes, and they are the key players in the regulation of cell-mediated immunity. We discuss how the nature of the DC maturation stimuli and the density and quality of DCs present in the T-cell areas of secondary lymphoid organs determine the magnitude and class of the T-cell response. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240143PMC
http://dx.doi.org/10.1186/ar567DOI Listing

The immunological synapse.

Authors:
Michael L Dustin

Arthritis Res 2002 9;4 Suppl 3:S119-25. Epub 2002 May 9.

Department of Pathology, New York University School of Medicine, Skirball Institute for Biomolecular Medicine, New York 10016, USA.

T-cell activation requires interaction of T-cell antigen receptors with proteins of the major histocompatibility complex (antigen). This interaction takes place in a specialized cell-cell junction referred to as an immunological synapse. The immunological synapse contains at least two functional domains: a central cluster of engaged antigen receptors and a surrounding ring of adhesion molecules. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240135PMC
http://dx.doi.org/10.1186/ar559DOI Listing

Endothelial activation: intracellular signaling pathways.

Authors:
Jordan S Pober

Arthritis Res 2002 9;4 Suppl 3:S109-16. Epub 2002 May 9.

Yale University School of Medicine, Boyer Center for Molecular Medicine, New Haven, CT 06510, USA.

Tumor necrosis factor (TNF) is the prototypic proinflammatory cytokine and endothelial cells are the principal cellular targets of its actions. Here I review the responses of endothelial cells to TNF, with emphasis on the induction of endothelial leukocyte adhesion molecules. I focus on the biochemistry and cell biology of signal transduction in TNF-treated endothelial cells that lead to the expression of adhesion molecules. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240152PMC
http://dx.doi.org/10.1186/ar576DOI Listing

VEGF and imaging of vessels in rheumatoid arthritis.

Authors:
Peter C Taylor

Arthritis Res 2002 9;4 Suppl 3:S99-107. Epub 2002 May 9.

The Kennedy Institute Division, Imperial College School of Medicine, London, UK.

Angiogenesis is a prominent feature of rheumatoid synovitis. Formation of new blood vessels permits a supply of nutrients and oxygen to the augmented inflammatory cell mass and so contributes to perpetuation of joint disease. Vascular endothelial growth factor (VEGF) is a potent endothelial cell-specific growth factor that is upregulated by proinflammatory cytokines and by hypoxia. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240157PMC
http://dx.doi.org/10.1186/ar582DOI Listing