ReportsImmunology

Reengineering chimeric antigen receptor T cells for targeted therapy of autoimmune disease

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Science  30 Jun 2016:
aaf6756
DOI: 10.1126/science.aaf6756

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  • The thresholds of activation for safe adoptive T cell therapy
    • Sebastian Kobold, Consultant in Clinical Pharmacology and Immunology, Klinikum der Universitaet Muenchen
    • Other Contributors:
      • Stefan Endres, Director of the Division of Clinical Pharmacology, Klinikum der Universitaet Muenchen

    Sebastian Kobold and Stefan Endres
    Center of Integrated Protein Science Munich (CIPS-M) and Division of Clinical Pharmacology, Department of Medicine IV, Klinikum der Universität München, Lindwurmstraße 2a, 80337 Munich, Germany, Member of the German Center for Lung Research (DZL); Sebastian.kobold@med.uni-muenchen.de; Tel: 0049-89440057300

    Ellebrecht et al. have recently reported on a concept to deplete antigen specific B cells through turning the pathogenic B cell receptor (BCR) into an agonistic molecule of adoptively transferred T cells (1). In this letter we want to highlight the importance of T cell activation by anti-desmoglein antibodies for safety considerations. The activation of T cells through agonistic multivalent molecules necessitates clustering of target transmembrane proteins on T cells (2, 3). It is dependent on the affinity of the agonist for its target protein which positively correlates with the degree of T cell activation (4, 5). Similar dependency holds true for chimeric antigen receptors (CAR) which potentially reflects the situation observed with the desmoglein fusion receptor (6). In the study by Ellebrecht et al., both BCR and its soluble form –the secreted immunoglobulin – are bivalent for the desmoglein fusion receptor and thus should both induce T cell activation. In fact, activation of transduced T cells was described in the study (Supplementary Figure 6B) but not deemed r...

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    Competing Interests: None declared.