Abstract

IntroductionRheumatoid arthritis (RA) is frequently complicated with infections. The aim of our study was to evaluate vaccination response in patients with RA after B-cell depletion by using rituximab.MethodsInfluenza (Afluria) and pneumococcal polysaccharides (Pneumo23) vaccines were given 6 months after rituximab (post-RTX group, n = 11) or 6 days before rituximab treatment (pre-RTX group; n = 8). RA patients never exposed to RTX composed the control group (n = 10). Vaccine-specific cellular responses were evaluated on day 6 after vaccination, and vaccine-specific humoral responses, on day 21.ResultsOn day 6 after vaccination, formation of influenza-specific B cells was lower in post-RTX group as compared with the pre-RTX group and controls (P = 0.04). Polysaccharide-specific B cells were found in 27% to 50%, being equally distributed between the groups. On day 21, the impairment of humoral responses was more pronounced with respect to influenza as compared with the pneumococcal vaccine and affected both IgG and light-chain production. Total absence of influenza-specific IgG production was observed in 55% of the post-RTX group.ConclusionsRTX compromises cellular and humoral vaccine responses in RA patients. However, repeated RTX treatment or previous anti-tumor necrosis factor (anti-TNF) treatment did not accentuate these defects.

Highlights

  • Rheumatoid arthritis (RA) is frequently complicated with infections

  • We evaluated the immunization response in RA patients treated with RTX 6 days after immunization and 6 months before immunization

  • We observed that RTX treatment impairs B-cell functions regarding cellular and humoral responses

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Summary

Introduction

Rheumatoid arthritis (RA) is frequently complicated with infections. The aim of our study was to evaluate vaccination response in patients with RA after B-cell depletion by using rituximab. Infections are one of the important causes of death in rheumatoid arthritis (RA) [1,2,3]. Antirheumatic treatment including conventional disease-modifying drugs and TNF inhibitors [6,7,8] may negatively affect the immunization response. Methotrexate (MTX), impairs optimal immunization response, whereas the effect of corticosteroids and azathioprine was less pronounced [9,10]. The combination of MTX and TNF inhibitors induces further deterioration of the immunization response [8]. The use of rituximab (RTX), a monoclonal antibody targeting CD20-expressing B cells, is an efficient novel strategy of RA treatment [11].

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