FRI0095 CHANGES IN B CELL PROFILE AS INDICATOR OF CLINICAL REMISSION TO TNF INHIBITORS IN PATIENTS WITH RHEUMATOID ARTHRITIS
Authors: Borja Hernández-Breijo, Israel Nieto-Gañán, Cristina Sobrino, Victoria Navarro-Compán, Ana Martínez-Feito, Carlota García-Hoz, Paloma Lapuente-Suanzes, Javier Bachiller-Corral, Gemma Bonilla, Cristina Pijoan Moratalla, Garbiñe Roy, Mónica Vázquez, Alejandro Balsa, Luisa María Villar, Dora Pascual-Salcedo, Eulalia Rodríguez-Martín, Chamaida Plasencia
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Rheumatoid arthritis (RA) is a chronic inflammatory disease with the typical characteristic of synovitis of small-sized and medium-sized joints that leads to cartilage and bone damage. TNF inhibitors (TNFi) are widely used for the treatment of rheumatoid arthritis (RA) however, there are still no objective indicators of clinical response to TNFi therapy. <h3>Objectives</h3> To analyse the change of peripheral blood mononuclear cells (PBMC) profile after 6 months (m) of treatment with TNFi in order to find cellular indicators of response. <h3>Methods</h3> Prospective bi-center pilot study including 100 RA patients receiving TNFi therapy. PBMC were isolated from patients at baseline and 6m of treatment, and were analysed by flow-cytometry. Clinical activity at baseline and 6m of TNFi treatment was assessed by DAS28. Clinical remission (DAS28≤2.6) after 6m of treatment was considered as optimal response. The association between clinical remission and the percentage of change (Δ, 6m-0m) within each PBMC subset was analysed through univariate logistic regression model (odds ratio; 95% CI; β; p-value). All the analyses were adjusted by sex, age, disease duration, concomitant-methotrexate, seropositivity (ACPA and/or Rheumatoid factor) and baseline-DAS28. <h3>Results</h3> Demographic characteristics before starting TNFi therapy are shown in Table 1. After 6m of TNFi treatment, 40% patients achieved clinical remission. Decreased percentage of B cells (ΔCD19+) was found after 6m of TNFi treatment in optimal responders, while suboptimal responders did not show differences with the baseline (OR: 0.78; 95% CI: 0.63-0.97; β: -0.25; p: 0.027) (Figure 1). This effect was essentially owing to a reduction of naïve B cells (OR: 0.76; 95% IC: 0.62-0.94; β: -0.27; p: 0.011) (Figure 1). No significant association was found between the other PBMC subsets (monocytes, NK cells, CD4+ T cells and CD8+ T cells) and clinical remission (Figure 1). <h3>Conclusion</h3> Our results suggest that B cells may be useful as a cellular indicator of response to TNFi in RA patients. <h3>Acknowledgement</h3> ISCIII (PI16/00474; PI16/01092) <h3>Disclosure of Interests</h3> Borja Hernández-Breijo: None declared, Israel Nieto-Gañán: None declared, Cristina Sobrino: None declared, Victoria Navarro-Compán: None declared, ANA MARTíNEZ-FEITO: None declared, Carlota García-Hoz: None declared, Paloma Lapuente-Suanzes: None declared, Javier Bachiller-Corral: None declared, Gemma Bonilla: None declared, Cristina Pijoan Moratalla: None declared, Garbiñe Roy: None declared, Mónica Vázquez: None declared, Alejandro Balsa Grant/research support from: Abbvie, Pfizer, Novartis, BMS, Nordic, Sanofi, Consultant for: Abbvie, Pfizer, Novartis, BMS, Nordic, Sanofi, Sandoz, Lilly, Paid instructor for: Pfizer, Speakers bureau: Pfizer, Novartis, UCB, Nordic, Sanofi, Sandoz, Lilly, Luisa María Villar: None declared, DORA PASCUAL-SALCEDO Grant/research support from: Pfizer, Speakers bureau: Pfizer, Abbvie, Takeda, Eulalia Rodríguez-Martín: None declared, Chamaida Plasencia Speakers bureau: Pfizer, MSD