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At least 19 recordsLinked to original sources
PubMed1978

Nitroblue tetrazolium test in psoriatic arthritis, rheumatoid arthritis, and osteoarthrosis.

Nitroblue tetrazolium test scores were obtained in 43 patients with psoriatic arthritis, 32 patients with rheumatoid arthritis, and 16 patients with osteoarthrosis. The mean score in all groups was similar and was higher than previously reported in patients awaiting heart surgery or with noninfective dermatoses. The test is not thought to be helpful in differentiating psoriatic arthritis from rheumatoid arthritis, and its usefulness in the diagnosis of septic arthritis superimposed on other forms of arthropathy is limited.

Arthritis↗
PubMed2025

Metagenomic Analysis of the Tonsil Virome Highlights Its Diagnostic Potential for Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease whose exact pathogenesis remains unclear, despite links to genetics, environmental factors, and microbial dysbiosis. Recent studies have highlighted the role of the microbiome in RA, yet the contribution of the tonsil virome remains unexplored. This study aims to investigate whether changes in the tonsil virome are associated with RA progression and assess its diagnostic potential. Using metagenomic data from 32 RA patients and 30 healthy controls (HCs), we identified 45 782 viral operational taxonomic units (vOTUs), with 14 341 classified as core vOTUs. RA patients exhibited significantly reduced virome richness and diversity, whereas Siphoviridae and Microviridae dominated both groups. Statistical analysis identified 235 RA-associated viral markers, including 13 enriched in RA and 222 in HCs. RA-enriched markers were primarily bacteriophages infecting Streptococcaceae, whereas HCs displayed more diverse viral-host interactions. Random forest models demonstrated strong discriminatory power of viral markers in distinguishing RA patients from HCs, achieving an AUC of 0.960, outperforming bacterial markers. Correlation analyses further linked viral markers to immune cell subsets, suggesting that tonsil virome alterations may influence immune dysregulation in RA. This study reveals significant changes in the tonsil virome of RA patients, highlighting its potential as a diagnostic tool and offering new insights into RA pathogenesis. These findings pave the way for future research into the virome's role in autoimmune diseases and therapeutic development.

Humans↗
PubMed2026

Proteomics-Based Identification of the Pyroptosis-Related Biomarker PCSK9 and Its Association With the Pathogenesis of Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a common autoimmune disease, and early diagnosis is critical for effective treatment. This study aims to identify potential biomarkers related to pyroptosis through serum proteomics analysis, offering new insights for the early diagnosis of RA. We enrolled 100 participants, including 50 patients with RA and 50 healthy controls. Serum samples were collected and analyzed using high-resolution liquid chromatography-tandem mass spectrometry (LC-MS/MS) for proteomics profiling. Differential protein expression analysis and functional annotation revealed significant upregulation of pyroptosis-related proteins in the serum of patients with RA. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, along with protein-protein interaction (PPI) network analysis, showed that these proteins are involved in inflammation and immune pathways, particularly the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome. Enzyme-linked immunosorbent assay (ELISA) validation confirmed a significant increase in PCSK9 levels in patients with RA, suggesting that PCSK9 may play a key role in the pathogenesis of RA. This study provides new directions for biomarker research in RA, particularly regarding the potential involvement of the pyroptosis pathway, with significant clinical application prospects.

Humans↗
PubMed2025

Immune Aging in Rheumatoid Arthritis.

Rheumatoid arthritis (RA) is a life-long autoimmune disease caused by the confluence of genetic and environmental variables that lead to loss of self-tolerance and persistent joint inflammation. RA occurs at the highest incidence in individuals >65 years old, implicating the aging process in disease susceptibility. Transformative approaches in molecular immunology and in functional genomics have paved the way for pathway paradigms underlying the replacement of immune homeostasis with autodestructive immunity in affected patients, including the process of immune aging. Patients with RA have a signature of premature immune aging, best understood for CD4+ T cells, which function as pathogenic effectors in this HLA class II-associated disease. Premature immune aging is present in healthy HLA-DRB1*04+ individuals, placing accelerated immune aging before joint inflammation. Aging-related molecular abnormalities directly implicated in turning RA CD4+ T cells into proinflammatory effector cells are linked to malfunction of subcellular organelles, such as mitochondria, lysosomes, lipid droplets, and the endoplasmic reticulum. Resulting changes in T cell behavior include cellular hypermobility, tissue invasiveness, unopposed mammalian target of rapamycin complex (mTORC)1 activation, excessive release of tumor necrosis factor, lysosomal failure, clonal expansion, and immunogenic cell death. Aged and metabolically reprogrammed T cells in patients with RA are accompanied by age-associated B cells, which specialize in autoantibody production. Clonal hematopoiesis drives myeloid cell aging by producing aged monocytes and hypermetabolic macrophages, which sustain the process of inflammaging. Here, we synthesize insights into the relationship of RA risk and immune aging and discuss mechanisms through which immune aging can cause autoimmunity.

Humans↗
PubMed1979

Differentiation between psoriatic arthritis and rheumatoid arthritis: a biochemical and statistical analysis of fingernail amino acids.

The differentiation between psoriatic arthritis and rheumatoid arthritis can be clinically difficult if there is no manifest psoriasis of skin or nail. In order to clarify this diagnostic problem, the amino acid patterns in seventy-five psoriatic and non-psoriatic nails have been studied. Using gas--liquid chromatographic techniques and discriminant analysis, a high degree of differentiation (96%) has been established between the normal looking nails of patients with psoriatic arthritis and those with rheumatoid arthritis. This biochemical/statistical approach to the fingernail enhances diagnosis in difficult clinical problems, particularly where there are no overt manifestations of psoriasis.

Amino Acids↗
PubMed1979

General mechanisms of inflammation in rheumatoid arthritis.

Rheumatoid synovitis is characterized by the simultaneous occurrence of two major types of immunologically-induced inflammation. These usually occur concurrently in the same joint. A cellular immune response is present in the sublining layer of the synovial membrane and an immune complex-induced acute inflammatory reaction is present in the synovial effusion phase of the disease. The two reactions are closely related and mutually interdependent. The cellular immune response is reduced in rheumatoid arthritis, but the chronic inflammatory cells of the synovium are active in the synthesis of IgG and probably considerable amounts of IgG rheumatoid factor. Rheumatoid factor complexes, particularly IgG-RF complexes, appear to be responsible for the exudative, immune complex-induced inflammatory phase of the disease.

Arthritis, Rheumatoid↗
PubMed1979

Cutaneous manifestations of rheumatoid arthritis.

Rheumatoid arthritis (RA) is a systemic illness defined and classified according to strict criteria of the American Rheumatism Association. Cutaneous disease may complicate RA or the drugs used in its treatment. Cutaneous vasculitis is potentially a prognostic factor in patients with RA. Controversy exists regarding the role of corticosteroids in the development of rheumatoid vasculitis. Two illustrative cases of RA with cutaneous complications are presented and the joint and cutaneous manifestations are reviewed herein.

Adrenal Cortex Hormones↗
PubMed1978

In vitro mitogen stimulation of synovial fluid lymphocytes from rheumatoid arthritis and juvenile rheumatoid arthritis patients: dissociation between the response to antigens and polyclonal mitogens.

The in vitro responses to mitogens of synovial fluid lymphocytes obtained from eight patients with rheumatoid arthritis (RA) and eight patients with juvenile rheumatoid arthritis (JRA) were studied. The results were compared to the transformation of the patient's peripheral blood lymphocytes stimulated with the same mitogens. Both RA and JRA synovial fluid lymphocytes showed a low transformation to the polyclonal mitogens PHA and PWM with a low ratio PHA-response/PWM-response. The stimulatory effect of purified protein derivative of tuberculin (PPD) was high, whereas a Candida albicans antigen preparation gave a more variable stimulation of the synovial fluid lymphocytes. In some patients the complete mitogen transformation profile of lymphocytes obtained from synovial fluid, synovial tissue and peripheral blood was studied. The results of the synovial fluid and tissue lymphocytes were similar.

Antigens↗
PubMed1977

Antibody-dependent cytotoxicity mediated by cells eluted from synovial tissues of patients with rheumatoid arthritis and juvenile rheumatoid arthritis.

Cell suspensions containing an average of 78% lymphocytes were obtained from synovial tissues of 26 patients with rheumatoid arthritis and 10 patients with juvenile rheumatoid arthritis. These cells were shown to mediate cytotoxicity against 51Cr-labeled chicken erythrocytes sensitized with a rabbit anti-chicken erythrocyte antiserum. Nylon column filtration of the cells increased the proportion of lymphocytes and usually also the cytotoxicity, which suggested that at least some of the effector cells were lymphocytes. The cytotoxic activity of the cells obtained from rheumatoid synovial tissue was always lower than that obtained with the patients' peripheral blood lymphocytes. No significant change in cytotoxicity of normal peripheral blood lymphocytes was observed after these cells had been treated in the same manner as the rheumatoid synovial tissues.

Antibody-Dependent Cell Cytotoxicity↗
PubMed2026

Serum Proteomic Signatures of Rheumatoid Arthritis Risk and Response: Analysis of a Rheumatoid Arthritis Interception Trial.

OBJECTIVE: Our study objective was to identify serum protein signatures associated with progression to rheumatoid arthritis (RA) and response to abatacept in at-risk individuals. METHODS: A total of 440 serum samples from 118 APIPPRA (Arthritis Prevention In the Preclinical Phase of RA with Abatacept) study participants were selected from baseline to RA onset for 46 progressors of RA or to study end for 72 participants who did not develop RA. Samples were analyzed using the SomaScan 7k assay platform. Differential expression analysis was assessed by progression to RA (three pre-RA time intervals to RA, progressors of RA vs nonprogressors, baseline to RA), and by treatment allocation (abatacept vs placebo). Risk and response signatures were identified in the full 7k panel and two prespecified subpanels defined as Inflammatory Mediators and Adaptive Immune Cell panel. RESULTS: We observed significant changes in 80 proteins (68 down-regulated and 12 up-regulated) occurring between RA onset and 6 to 24 months before developing disease. Progression to RA was associated with increased levels of acute-phase reactants SAA1 and SAA2 and reductions in CTLA4, when compared to nonprogressors at the end of treatment. Two up-regulated proteins (CTLA4 and CD86) and seven down-regulated proteins (CXCL13, FCRL4, FCER2, CCL21, LTA|LTB, FDCSP, and IL22RA2) were observed in participants receiving abatacept compared to placebo regardless of RA outcome. CONCLUSION: Protein signatures dominated by acute-phase proteins define progression to RA, whereas changes associated with abatacept therapy highlight potential mechanisms of treatment response. Such signatures provide a better understanding of the immune landscape of the at-risk phase, opening up the possibility of new treatment modalities for RA prevention.

Adult↗
PubMed1979

Viruses and lymphocytes in rheumatoid arthritis. II. Examination of lymphocytes and sera from patients with rheumatoid arthritis for evidence of retrovirus infection.

The possible involvement of retroviruses in the aetiology of rheumatoid arthritis (RA) was investigated. Retrovirus antigens were not expressed on rheumatoid synovial and peripheral blood lymphocytes as judged by membrane immunofluorescence, radioimmunoassay, and complement-mediated cytotoxicity. The specific antiretroviral (anti-RD-144 and anti-SSAV) sera used in this study were produced in rabbits immunised with viral antigens grown in a homologous system (rabbit cells and medium supplemented with normal rabbit serum), avoiding non-specific immunofluorescence previously detected with donated antiretroviral sera. Immune complexes lodged in the rheumatoid synovial membranes did not contain, and other cells within the membranes did not express, retroviral antigens. Antibodies cross-reacting with primate retrovirus antigens were sought in sera from patients with 'autoimmune' diseases by means of solid phase radioimmunoassay. There were no retrovirus antibodies in the 3 groups of patients studied, that is, those with rheumatoid arthritis, systemic lupus erythematosus, and with non-RA conditions. Absorption of rheumatoid factor did not alter this conclusion. These results give little support to the hypothesis that activation of endogenous human retroviruses or an infection with horizontally transmitted retroviruses is associated with the rheumatoid process.

Antigens, Surface↗