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Open Access Highly Accessed Research article

Decreased influenza-specific B cell responses in rheumatoid arthritis patients treated with anti-tumor necrosis factor

James J Kobie1, Bo Zheng1, Peter Bryk1, Michael Barnes2, Christopher T Ritchlin1, Darren A Tabechian1, Allen P Anandarajah1, R John Looney1, Ralf G Thiele1, Jennifer H Anolik1, Andreea Coca1, Chungwen Wei1, Alexander F Rosenberg1, Changyong Feng3, John J Treanor4, F Eun-Hyung Lee2 and Ignacio Sanz1*

Author Affiliations

1 Division of Allergy, Immunology and Rheumatology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 695, Rochester, NY, 14642, USA

2 Division of Pulmonary & Critical Care Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 692, Rochester, NY, 14642, USA

3 Department of Biostatistics and Computational Biology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 630, Rochester, NY, 14642, USA

4 Division of Infectious Disease, University of Rochester Medical Center, 601 Elmwood Avenue, Box 689, Rochester, NY, 14642, USA

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Arthritis Research & Therapy 2011, 13:R209  doi:10.1186/ar3542

Published: 16 December 2011

Abstract

Introduction

As a group, rheumatoid arthritis (RA) patients exhibit increased risk of infection, and those treated with anti-tumor necrosis factor (TNF) therapy are at further risk. This increased susceptibility may result from a compromised humoral immune response. Therefore, we asked if short-term effector (d5-d10) and memory (1 month or later) B cell responses to antigen were compromised in RA patients treated with anti-TNF therapy.

Methods

Peripheral blood samples were obtained from RA patients, including a subset treated with anti-TNF, and from healthy controls to examine influenza-specific responses following seasonal influenza vaccination. Serum antibody was measured by hemagglutination inhibition assay. The frequency of influenza vaccine-specific antibody secreting cells and memory B cells was measured by EliSpot. Plasmablast (CD19+IgD-CD27hiCD38hi) induction was measured by flow cytometry.

Results

Compared with healthy controls, RA patients treated with anti-TNF exhibited significantly decreased influenza-specific serum antibody and memory B cell responses throughout multiple years of the study. The short-term influenza-specific effector B cell response was also significantly decreased in RA patients treated with anti-TNF as compared with healthy controls, and correlated with decreased influenza-specific memory B cells and serum antibody present at one month following vaccination.

Conclusions

RA patients treated with anti-TNF exhibit a compromised immune response to influenza vaccine, consisting of impaired effector and consequently memory B cell and antibody responses. The results suggest that the increased incidence and severity of infection observed in this patient population could be a consequence of diminished antigen-responsiveness. Therefore, this patient population would likely benefit from repeat vaccination and from vaccines with enhanced immunogenicity.