Rheumatoid Arthritis Awareness Day is observed annually on 2 February and is a vital initiative aimed at spreading awareness about rheumatoid arthritis, an autoimmune disease that affects millions of people worldwide.
In this blog the Cellomatics team discuss the disease and how we study it using a multi-parametric approach to provide deeper insight.
Rheumatoid Arthritis (RA) is a chronic autoimmune disease characterised by persistent inflammation of the synovial joints. Immune-mediated attack on joint tissues leads to pain, swelling, stiffness, and progressive joint destruction, often resulting in irreversible functional impairment. Beyond the joints, RA is a systemic condition that can affect major organs including the heart, kidneys, muscles, and bones.
Although there is currently no cure, early diagnosis and appropriate intervention can significantly reduce disease activity, slow progression, and improve quality of life through a combination of pharmacological treatment and lifestyle modification.
The term Rheumatoid Arthritis was first introduced by Alfred B. Garrod in 1858 to distinguish the condition from osteoarthritis [1]. In the United Kingdom, RA affects approximately 400,000 adults and is two to three times more prevalent in women than in men. Disease onset and progression are influenced by both genetic susceptibility and environmental factors, including smoking and dietary components.
Over the past two decades, research supported by organisations including Arthritis UK has contributed to the development of biological therapies such as TNF inhibitors (e.g., adalimumab) [2]. These targeted treatments interrupt specific inflammatory pathways and have revolutionised RA management, particularly for individuals who do not respond sufficiently to first‑line Disease‑Modifying Anti‑Rheumatic Drugs (DMARDs).
However, RA remains a complex disease involving multiple cell types, cytokine networks, and oxidative stress pathways. This complexity demands robust laboratory models capable of capturing the multifaceted biology of RA.
At Cellomatics, we recognise that effective RA modelling requires more than a single experimental endpoint. Our multi-parametric approach integrates diverse cellular, molecular, and functional readouts, to provide a comprehensive understanding of disease biology. This strategy provides deeper insight into inflammatory cascades, immune cell interactions, and tissue-destructive processes central to RA.
In recognition of Rheumatoid Arthritis Awareness Day, we highlight our laboratory studies examining inflammatory signalling and oxidative stress across multiple RA-relevant cell systems. These investigations assess cytokine-driven inflammation and reactive oxygen species (ROS) production in Human fibroblast-like synoviocytes (FLS) and Immune cell co-culture systems.
Fibroblast-like synoviocytes play a central role in RA pathogenesis, contributing to synovial hyperplasia, cytokine release, and cartilage degradation. To better reflect the inflammatory microenvironment of the RA joint, we assessed interleukin-1β (IL-1β)–induced inflammatory responses in co-cultures of human FLS and peripheral blood mononuclear cells (PBMCs).
In this system, FLS were pre-treated with the small-molecule inhibitor Lorecivivint (30 μM) prior to cytokine stimulation (Figure 1). This approach enabled evaluation of pathway modulation within a physiologically relevant, immune-interactive context.
Figure 1: Cytokine and ROS levels in IL‑1β–stimulated Fibroblast-like Synoviocytes (FLS):PBMC co‑cultures from health donors. Co‑cultures were stimulated with IL‑1β for 24 h (red) or 48 h (blue), with FLS pre‑treated with Lorecivivint (30 µM). Panel A: TNFα, IFNγ, IL‑2 and IL‑6 were quantified by Luminex, and cellular Panel B: ROS by plate‑reader assay. Data are mean ± SEM of triplicates; significance versus IL‑1β controls by one‑way ANOVA/Dunnett’s test (*p ≤ 0.05; **p ≤ 0.01; **p ≤ 0.001).
Rheumatoid arthritis – Frequently asked questions
Why can this autoimmune joint condition become serious over time?
Rheumatoid arthritis is a chronic autoimmune inflammatory disease that progressively damages healthy joint tissue, leading to inflammation, pain, swelling, and loss of joint function. In more severe cases, it can also affect other organs, including the skin, lungs, blood vessels, and cardiovascular system.
Why is this Arthritis form so hard to manage?
Rheumatoid arthritis is a complex immuno-inflammatory disease involving dysregulated immune responses and chronic joint inflammation. Over time, persistent inflammation can lead to joint stiffness, cartilage damage, reduced mobility, and a significant impact on quality of life.
How do researchers study this type of Arthritis in the laboratory?
Researchers use a range of in vitro models and cellular assays, including primary healthy or disease-derived chondrocytes and fibroblast-like synoviocytes, often in combination with immune cells, to investigate inflammatory pathways, immune signalling, and tissue responses associated with rheumatoid arthritis. These systems support mechanistic studies and the evaluation of potential therapeutic compounds during preclinical research
Which biomarkers monitor this type of Arthritis?
Common biomarkers include inflammatory cytokines such as TNF-α, IL-6, and IL-1β, along with immune signalling markers and proteins associated with joint inflammation and tissue remodelling. These biomarkers are widely used to monitor disease activity and therapeutic
response.
How does Rheumatoid Arthritis support drug discovery?
Rheumatoid arthritis models are widely used to evaluate compounds targeting inflammation, immune dysregulation, and joint destruction. Advanced screening platforms support rapid assessment of therapeutic candidates and help accelerate preclinical drug discovery programmes.
