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  Chronic lymphocytic leukaemia is driven by antigen-independent cell-autonomous signalling

Dühren-von Minden, M., Übelhart, R., Schneider, D., Wossning, T., Bach, M. P., Buchner, M., et al. (2012). Chronic lymphocytic leukaemia is driven by antigen-independent cell-autonomous signalling. Nature, 489, 309-312.

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Dühren-von Minden, Marcus1, Autor           
Übelhart, Rudolf1, Autor           
Schneider, Dunja1, Autor           
Wossning, Thomas1, Autor           
Bach, Martina P.1, Autor           
Buchner, Maike, Autor
Hofmann, Daniel2, Autor
Surova, Elena1, Autor           
Follo, Marie, Autor
Köhler, Fabian1, Autor           
Wardemann, Hedda, Autor
Zirlik, Katja, Autor
Veelken, Hendrik, Autor
Jumaa, Hassan1, Autor           
Affiliations:
1Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243645              
2Max Planck Society, ou_persistent13              

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 Zusammenfassung: B-cell antigen receptor (BCR) expression is an important feature of chronic lymphocytic leukaemia (CLL), one of the most prevalent B-cell neoplasias in Western countries. The presence of stereotyped and quasi-identical BCRs in different CLL patients suggests that recognition of specific antigens might drive CLL pathogenesis. Here we show that, in contrast to other B-cell neoplasias, CLL-derived BCRs induce antigen-independent cell-autonomous signalling, which is dependent on the heavy-chain complementarity-determining region (HCDR3) and an internal epitope of the BCR. Indeed, transferring the HCDR3 of a CLL-derived BCR provides autonomous signalling capacity to a non-autonomously active BCR, whereas mutations in the internal epitope abolish this capacity. Because BCR expression was required for the binding of secreted CLL-derived BCRs to target cells, and mutations in the internal epitope reduced this binding, our results indicate a new model for CLL pathogenesis, with cell-autonomous antigen-independent signalling as a crucial pathogenic mechanism.

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Sprache(n): eng - English
 Datum: 2012
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: eDoc: 633314
 Art des Abschluß: -

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Titel: Nature
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 489 Artikelnummer: - Start- / Endseite: 309 - 312 Identifikator: -