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

Author

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, and Bonnotte, Bernard

Published
2013
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2. Preferential splenic CD8+ T-cell activation in rituximab-nonresponder patients with immune thrombocytopenia

Author

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

Subjects
Adult, Male, Immunology, Drug Resistance, Spleen, CD8-Positive T-Lymphocytes, Lymphocyte Activation, Real-Time Polymerase Chain Reaction, Biochemistry, Pathogenesis, Antibodies, Monoclonal, Murine-Derived, Young Adult, immune system diseases, hemic and lymphatic diseases, medicine, Humans, Immunologic Factors, Cytotoxic T cell, Aged, Aged, 80 and over, Purpura, Thrombocytopenic, Idiopathic, biology, business.industry, Cell Biology, Hematology, T lymphocyte, Middle Aged, Immunohistochemistry, medicine.anatomical_structure, Monoclonal, biology.protein, Female, Rituximab, Antibody, business, CD8, medicine.drug
Abstract

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(+) T-cell frequency. Moreover, in the RTX- nonresponder patient group, the CD8(+) T-cell repertoire displays a restricted pattern. In the blood, the phenotype of CD8(+) 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(+) T cells in ITP patients who did not respond to RTX and suggest their involvement in platelet destruction in these patients.

Published
2013
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3. Preferential splenic CD8+T-cell activation in rituximab-nonresponder patients with immune thrombocytopenia

Author

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, and Bonnotte, Bernard

Abstract

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+T-cell frequency. Moreover, in the RTX- nonresponder patient group, the CD8+T-cell repertoire displays a restricted pattern. In the blood, the phenotype of CD8+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+T cells in ITP patients who did not respond to RTX and suggest their involvement in platelet destruction in these patients.

Published
2013
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4. Preferential splenic CD8+ T-cell activation in rituximab-nonresponder patients with immune thrombocytopenia.

Author

Audia, Sylvain, Samson, Maxime, Mahevas, 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, Agnes, Michel, Marc, Godeau, Bertrand, and Larmonier, Nicolas

Subjects
*THROMBOCYTOPENIA, *CELLULAR therapy, *BLOOD platelet disorders, *T cells, *HEMATOPOIETIC system
Abstract

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+ T-cell frequency. Moreover, in the RTX- nonresponder patient group, the CD8+ T-cell repertoire displays a restricted pattern. In the blood, the phenotype of CD8+ 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+ T cells in ITP patients who did not respond to RTX and suggest their involvement in platelet destruction in these patients [ABSTRACT FROM AUTHOR]

Published
2013
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