Abstract
Biological therapies, such as TNF inhibitors (TNFi), are increasing remission (REM) rates in rheumatoid arthritis (RA) patients, although these are still limited. The aim of our study was to analyze changes in the profile of peripheral blood mononuclear cells (PBMC) in patients with RA treated with TNFi in relation to the clinical response. This is a prospective and observational study including 78 RA patients starting the first TNFi. PBMC were analyzed by flow cytometry both at baseline and at 6 months. Disease activity at the same time points was assessed by DAS28, establishing DAS28 ≤ 2.6 as the criteria for REM. Logistic regression models were employed to analyze the association between the changes in PBMC and REM. After 6 months of TNFi treatment, 37% patients achieved REM by DAS28. Patients who achieved REM showed a reduction in the percentage of naive B cells, but only when patients had received concomitant methotrexate (MTX) (OR: 0.59; 95% CI: 0.39–0.91). However, no association was found for patients who did not receive concomitant MTX (OR: 0.85; 95% CI: 0.63–1.16). In conclusion, PBMC, mainly the B-cell subsets, are modified in RA patients with TNFi who achieve clinical REM. A significant decrease in naive B-cell percentage is associated with achieving REM after 6 months of TNFi treatment in patients who received concomitant therapy with MTX.
Highlights
Tumor necrosis factor inhibitors (TNFi) are widely used for the treatment of patients with rheumatoid arthritis (RA), who do not respond to conventional synthetic disease-modifying antirheumatic drugs
We aimed to investigate how peripheral blood cell profile can be modified after TNFi treatment, according to the clinical response in patients with RA
The results showed that a reduction in the percentage of peripheral naive B cells was associated with attaining REM in patients with RA treated with TNFi, mainly in combination with MTX
Summary
Tumor necrosis factor inhibitors (TNFi) are widely used for the treatment of patients with rheumatoid arthritis (RA), who do not respond to conventional synthetic disease-modifying antirheumatic drugs (csDMARDs). B Cells and TNFi Treatment of the molecular mechanisms underlying the effect of TNFi therapy, there is still a lack of objective parameters associated with clinical response to TNFi in RA [2, 3]. It is well-known that different types of immune cells such as monocytes and natural killer (NK), T, and B cells are involved in the development of inflammation and autoimmunity in the RA pathogeny [4,5,6]. To deepen into this field, more studies are needed [13]
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