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AB0041 B-cell activating factor (BAFF) binding receptors (BBR) on B cells: characterization in patients with rheumatoid arthritis (RA) receiving anti-TNF-alpha agent infliximab (IFX)
  1. D. Hernández1,
  2. I.D. de la Torre1,
  3. G. Cambridge2,
  4. L. Martinez1,
  5. J.C. Nieto1,
  6. J. Ovalles1,
  7. J. Barrios1,
  8. C. González1,
  9. M. Montoro1,
  10. J. Lόpez-Longo1,
  11. I. Monteagudo1,
  12. L. Carreño1,
  13. L. Valor1
  1. 1Rheumatology, Gregorio Marañόn Hospital, Madrid, Spain
  2. 2Rheumatology, University College of London, London, United Kingdom


Objectives To evaluate BBR (BAFF-R, TACI and BCMA) expression on B-cells in response to the treatment with the anti-TNF-alpha agent infliximab in RA patients

Methods We assessed naïve and memory B-cells expressing BBR in peripheral blood in 23 patients with RA on infliximab treatment: 12 in no-remission (DAS28>3.2), 11 in remission (DAS28<2.6) and healthy controls (HC; n=12) using monoclonal antibodies to CD19, CD27, IgD, CD38, BAFF-R, TACI and BCMA by multiparametric flow cytometry.

Results Despite similar BAFF-R expression on naïve and memory B-cells of RA patients (remission/no-remission) compared to HC, we found increased % of CD27+ memory B-cells TACI+ in RA patients (remission/non remission) compared to HC (p=0.004 and p=0.01, respectively). A significantly lower % of B-cells expressed BCMA on naive population for both remission/ no-remission RA patients vs. HC (naïve mature, CD19+IgD++CD38-, p=0.01 and p=0.001, respectively, naïve transitional CD19+IgD+,CD38++,p=0.0007 and p=0.01, respectively) and on memory population only for RA patients in remission compared to HC (plasmablast CD19+IgD-CD38 p=0.03, and post-GC memory CD19+,IgD-CD38++, p=0.04).

Conclusions Major BBR alterations are present in RA patients treated with the anti-TNF agent infliximab; blocking TNF-alpha could restore partly the defect on the maturation-survival process in RA patients B-cells, down-regulating BCMA and preventing short lived B-cells from becoming antibody-producing plasma cells. However, RA patients on anti-TNF therapy show a increased TACI and decreased BCMA expression in memory B-cells; defects in B-cell pool might persist due to contributions by other soluble and/or cellular mediators.

Disclosure of Interest None Declared

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