Rheumatoid arthritis is a long-term inflammatory disease that affects the synovial tissue of various joints. High concentrations of acute-phase reactants, autoantibodies and erosions on radiographs, as well as the number of affected joints and the nature of the lesion, are used to make the diagnosis.

In addition to the significant heterogeneity among RA patients with regard to leukocyte invasion of the joints and activation of inflammation-related genes. Inter-individual differences in gene signatures are observed in peripheral blood and synovial tissue. For example, higher levels of expression of IFN type I controlled genes were found in the peripheral blood of almost half of patients with RA, consistent with triggering a pathogen response programme. The discrepancy between people with measurable anti-citrullinated peptide antibodies (ACPA) and those who are ACPA-negative significantly supports the idea that RA should be considered as a syndrome involving more than one pathogenetic unit.

Common end-paths are influenced by effective anti-rheumatic therapies. The fact that clinical arthritis activity is accompanied by persisting humanized antibodies against cluster differentiation 52 (CD52) or CD4 antibodies after therapy, despite significant depletion of peripheral blood lymphocytes, serves as an illustration of the importance of collecting data on synovia, the leading inflammatory focus, for understanding the effects of antirheumatic treatment.

In order to improve responsiveness, preserve joint structural and functional characteristics, and reduce treatment costs, there is an urgent need for reliable biomarkers that are associated with the response to biological therapy. It is now possible to predict how well rituximab will work as a therapy because of the various clinical signs associated with how the body will respond to TNF suppression and the presence of antibodies in the blood. Lack of response cannot be predicted, but existing response markers can predict the likelihood of response to the drug or the quality of response.