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).
