ReviewClinical reviews in allergy & immunology2016
Inflammatory Cell Migration in Rheumatoid Arthritis: A Comprehensive Review.
Review in Clinical reviews in allergy & immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 99 citations in OpenAlex.
- Dynamic insights into cellular mechanics and membrane undulations in vascular smooth muscle cells.American journal of physiology. Cell physiology · 2026Article
- Nanoparticle Delivery Systems in Rheumatoid Arthritis: More Than Vehicles.Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2026Review
- Identification of diagnostic genes in rheumatoid arthritis using integrated bioinformatics, machine learning, and experimental validation.Frontiers in medicine · 2026Article
- The multiple functions of CD5 in diseases related to immune disorders.Annals of medicine · 2025Review
- Microenvironment-driven transformable self-assembly nanoplatform enables spatiotemporal remodeling for rheumatoid arthritis therapy.Science advances · 2025Article
- Deep-insights: Nanoengineered gel-based localized drug delivery for arthritis management.Asian journal of pharmaceutical sciences · 2025Review
- Conventional Tregs in treatment-naïve rheumatoid arthritis are deficient in suppressive function with an increase in percentage of CXCR3 and CCR6 expressing Tregs.Immunologic research · 2024Article
- A dual dynamically cross-linked hydrogel promotes rheumatoid arthritis repair through ROS initiative regulation and microenvironment modulation-independent triptolide release.Materials today. Bio · 2024Article
- Receptors expressions on peripheral lymphocytes and CD4Immunity, inflammation and disease · 2023Article
- Integrative network fusion-based multi-omics study for biomarker identification and patient classification of rheumatoid arthritis.Chinese medicine · 2023Article
- Sandwich Culture Platforms to Investigate the Roles of Stiffness Gradients and Cell-Matrix Adhesions in Cancer Cell Migration.Cancers · 2023Article
- Serum amyloid A proteins reduce bone mass during mycobacterial infections.Frontiers in immunology · 2023Article
- Identification and Development of Synovial B-Cell-Related Genes Diagnostic Signature for Rheumatoid Arthritis.Journal of immunology research · 2023Article
- Bone erosion in inflammatory arthritis is attenuated byiScience · 2022Article
- Hypoxia-Inducible Factor-2 Alpha Regulates the Migration of Fibroblast-like Synoviocytes via Oxidative Stress-Induced CD70 Expression in Patients with Rheumatoid Arthritis.International journal of molecular sciences · 2022Article
- Article
- Adenosine deaminase modulates metabolic remodeling and orchestrates joint destruction in rheumatoid arthritis.Scientific reports · 2021Article
- ZIP8 exacerbates collagen-induced arthritis by increasing pathogenic T cell responses.Experimental & molecular medicine · 2021Article
- Microbial Lipid A Remodeling Controls Cross-Presentation Efficiency and CD8 T Cell Priming by Modulating Dendritic Cell Function.Infection and immunity · 2021Article
- Cross-Tissue Transcriptomic Analysis Leveraging Machine Learning Approaches Identifies New Biomarkers for Rheumatoid Arthritis.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that primarily affects the joints. Self-reactive B and T lymphocytes cooperate to promote antibody responses against self proteins and are major drivers of disease. T lymphocytes also promote RA independently of B lymphocytes mainly through the production of key inflammatory cytokines, such as IL-17, that promote pathology. While the innate signals that initiate self-reactive adaptive immune responses are poorly understood, the disease is predominantly caused by inflammatory cellular infiltration and accumulation in articular tissues, and by bone erosions driven by bone-resorbing osteoclasts. Osteoclasts are giant multinucleated cells formed by the fusion of multiple myeloid cells that require short-range signals, such as the cytokines MCSF and RANKL, for undergoing differentiation. The recruitment and positioning of osteoclast precursors to sites of osteoclast differentiation by chemoattractants is an important point of control for osteoclastogenesis and bone resorption. Recently, the GPCR EBI2 and its oxysterol ligand 7a, 25 dihydroxycholesterol, were identified as important regulators of osteoclast precursor positioning in proximity to bone surfaces and of osteoclast differentiation under homeostasis. In chronic inflammatory diseases like RA, osteoclast differentiation is also driven by inflammatory cytokines such as TNFa and IL-1, and can occur independently of RANKL. Finally, there is growing evidence that the chemotactic signals guiding osteoclast precursors to inflamed articular sites contribute to disease and are of great interest. Furthering our understanding of the complex osteoimmune cell interactions should provide new avenues of therapeutic intervention for RA.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.