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© Institut Pasteur
Structure de macromolécules : dimère d'aquométhémoglobine de cheval. Dérivé toxique oxydé de l'hémoglobine, représentant 1 à 2% du total.
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The Journal of clinical investigation - 03 May 2022

Canales-Herrerias P, Crickx E, Broketa M, Sokal A, Chenon G, Azzaoui I, Vandenberghe A, Perima A, Iannascoli B, Richard-Le Goff O, Castrillon C, Mottet G, Sterlin D, Robbins A, Michel M, England P, Millot GA, Eyer K, Baudry J, Mahevas M, Bruhns P,

Link to Pubmed [PMID] – 35503254

Link to DOI – 10.1172/JCI153580

J Clin Invest 2022 May; ():

The major therapeutic goal for immune thrombocytopenia (ITP) is to restore normal platelet counts using drugs to promote platelet production or by interfering with mechanisms responsible for platelet destruction. 80% of patients possess anti-integrin αIIbβ3 (GPIIbIIIa) IgG autoantibodies causing platelet opsonization and phagocytosis. The spleen is considered the primary site of autoantibody production by autoreactive B cells and platelet destruction. The immediate failure in ~50% of patients to recover a normal platelet count after anti-CD20 Rituximab-mediated B cell depletion and splenectomy suggest that autoreactive, rituximab-resistant, IgG-secreting B cells (IgG-SC) reside in other anatomical compartments. We analyzed >3,300 single IgG-SC from spleen, bone marrow and/or blood of 27 patients with ITP revealing high inter-individual variability in affinity for GPIIbIIIa with variations over 3 logs. IgG-SC dissemination and range of affinities were however similar per patient. Longitudinal analysis of autoreactive IgG-SC upon treatment with anti-CD38 mAb daratumumab demonstrated variable outcomes, from complete remission to failure with persistence of high-affinity anti-GPIIbIIIa IgG-SC in the bone marrow. This study demonstrates the existence and dissemination of high-affinity autoreactive plasma cells in multiple anatomical compartments of patients with ITP that may cause the failure of current therapies.

https://pubmed.ncbi.nlm.nih.gov/35503254