Preferential splenic CD8 1 T-cell activation in rituximab-nonresponder patients with immune thrombocytopenia

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Audia, Sylvain | Samson, Maxime | Mahévas, Matthieu | Ferrand, Christophe | Trad, Malika | Ciudad, Marion | Gautheron, Alexandrine | Seaphanh, Famky | Leguy, Vanessa | Berthier, Sabine | Salles, Bruno | Martin, Laurent | Lorcerie, Bernard | Ortega-Deballon, Pablo | Facy, Olivier | Caillot, Denis | Soudry-Faure, Agnès | Michel, Marc | Godeau, Bertrand | Larmonier, Nicolas | Saas, Philippe | Janikashvili, Nona | Bonnotte, Bernard

Edité par CCSD ; American Society of Hematology -

International audience. The pathogenic role of B cells in immune thrombocytopenia (ITP) has justified the therapeutic use of anti-CD20 antibodies such as rituximab (RTX). However, 60% of ITP patients do not respond to RTX. To decipher the mechanisms implicated in the failure of RTX, and because the spleen plays a well-recognized role in ITP pathogenesis, 12 spleens from ITP patients who had been nonresponders to RTX therapy were compared with 11 spleens from RTX-untreated ITP patients and 9 controls. We here demonstrate that in RTX-nonresponder ITP patients, preferential Th1 and Tc1 T lymphocyte polarizations occur, associated with an increase in splenic effector memory CD8 1 T-cell frequency. Moreover, in the RTX-nonresponder patient group, the CD8 1 T-cell repertoire displays a restricted pattern. In the blood, the phenotype of CD8 1 T cells before and after RTX treatment is not modified in responders or nonresponders. Altogether, these results demonstrate for the first time an activation of splenic CD8 1 T cells in ITP patients who did not respond to RTX and suggest their involvement in platelet destruction in these patients.

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