SAT0102 Rituximab-Induced T-Cell Depletion in Patients with Rheumatoid Arthritis: Association With Clinical Response

Objectives Rituximab, a monoclonal antibody specifically targeting CD20, induces B-cell depletion and is effective in rheumatoid arthritis (RA). We aimed to study whether routine monitoring of lymphocyte subpopulations, especially T cells, may be useful in patients receiving rituximab for RA. Methods We examined data for all patients receiving rituximab between July 2007 and November 2012 in our centre. Peripheral blood CD3 + , CD4 + , CD8 + , CD3 - CD56 + and CD19 + lymphocyte counts before and during the first course of rituximab were measured by flow cytometry. Mann-Whitney non-parametric test was used to compare lymphocyte subpopulation counts before and during treatment. Results We examined data for 75 patients (64 with RA, 11 with other inflammatory diseases). Rituximab induced unexpected and substantial depletion of T cells, mainly CD4 + cells, in most patients. The CD4 + count was 80% of the initial count, and was ≤ 200 CD4 + cells/mL in some patients. Importantly, lack of CD4 + cell depletion was associated with no clinical response, so the mechanism of action of rituximab may depend at least in part on T cells. Conclusions Rituximab induces substantial T-cell depletion mainly CD4+ cells, which is associated with the clinical response in RA. Routine monitoring of T cells may be useful in the clinical setting in inflammatory diseases. Acknowledgements The authors thank Drs Saloua Mammou, Isabelle Griffoul, Emilie Ducourau, and Virginie Martaille for helping in clinical assessment. We are indebted to Nelly Jaccaz-Vallee, Sergine Gosset, Valerie Angebeau, Laetitia Cornec, Adeline Coutellier, Corinne Depont, Vanessa Fougeray, Valerie Fuseau, Pascale Guibout, Sophie Joncheray, Celine Letot, Isabelle Romier and Elodie Vigneron for blood sampling and their commitment in taking care of patients and to Claude Gautier and Elisabeth Billant who performed blood sample staining and flow cytometry analysis. Disclosure of Interest J. Melet: None Declared, D. Mulleman Grant/research support from: Abbott, Roche, BMS, Pfizer, UCB and MSD, Consultant for: MSD and Pfizer, P. Goupille Grant/research support from: Abbott, Roche, BMS, Lilly, Novartis, Pfizer, UCB and MSD, Consultant for: Abbott, BMS, MSD, Pfizer, UCB, B. Ribourtout: None Declared, H. Watier: None Declared, G. Thibault: None Declared