Abstract
Tumour necrosis factor (TNF)-α is a key mediator of inflammation in rheumatoid arthritis, and its discovery led to the development of highly successful anti-TNF therapy. Subsequently, other biologic drugs targeting immune pathways, namely interleukin-6 blockade, B cell depletion, and T cell co-stimulation blockade, have been developed. Not all patients respond to a biologic drug, leading to a knowledge gap between biologic therapies available and the confident prediction of response. So far, genetic studies have failed to uncover clinically informative biomarkers to predict response. Given that the targets of biologics are immune pathways, immunological study has become all the more pertinent. Furthermore, advances in single-cell technology have enabled the characterization of many leucocyte subsets. Studying the blood immunophenotype may therefore, define biomarker profiles relevant to each individual patient’s disease and treatment outcome. This review summarises our current understanding of how immune biomarkers might be able to predict treatment response to biologic drugs.
Highlights
Rheumatoid arthritis (RA) is a highly heterogeneous autoimmune disease characterised by inflammation of synovial joints with a prevalence of 0.5–1% and an incidence of 20–50 per 100,000 annually [1]
Cells and Tregs, and binds the co-stimulatory molecules CD80 and CD86 found on antigen-presenting cells (APCs) with greater affinity than their ligand CD28, which is required for T cell receptor (TCR)
A regression model using clinical predictors of golimumab found that male gender, younger age, lower health assessment questionnaire (HAQ), erythrocyte sedimentation rate (ESR)/C-reactive peptide (CRP), tender joint count (TJC)/swollen joint count (SJC), and the absence of co-morbidities, could estimate remission rate using 3000 real-world patients [21]
Summary
Rheumatoid arthritis (RA) is a highly heterogeneous autoimmune disease characterised by inflammation of synovial joints with a prevalence of 0.5–1% and an incidence of 20–50 per 100,000 annually [1]. The heterogeneity of RA is becoming clearer as more evidence supports that the diagnosis encompasses a number of genetically related diseases that share joint inflammation as the presenting feature [2]. Structural joint damage leads to permanent disability which is detrimental to both the individual and societally [4]. The personalised approach will likely involve clinical, genetic, immunological, and hitherto unknown factors to inform treatment choice.
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