It is generally acknowledged that pathological B-cell receptors drive chronic lymphocytic leukaemia (CLL) via continuous signalling emanating from BCR-BCR homotypic interactions, rather than external antigens. Here the authors show, by analysing the structure and function of three B-cell receptors from patients with stereotyped CLL subset 1 that homotypic interactions and consequential autonomous signalling is not universal and other mechanisms could play roles in leukemic proliferation of CLL cells.
- Paolo G. Cocomazzi
- Anastasia Iatrou
- Massimo Degano
